#S-acetyl l-Glutathione

[vincosupplements]

The Benefits of S-acetyl l-Glutathione

If you want to get a highly effective supplement for the liver, S-acetyl l-Glutathione is the best product for you. Now easily available at our website. Give *immune support *DNA cell protection *Reduce inflammation and more benefits.

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Achieve Peak Performance with Andarine (S-4) by Magnus

Are you ready to elevate your muscle growth, strength, and overall performance? Andarine (S-4) by Magnus Pharmaceuticals is the ultimate supplement designed to help you achieve your fitness goals more effectively. This powerful formula combines potent ingredients that work synergistically to boost muscle gains, improve strength, and support overall well-being. Let’s explore the active ingredients in Andarine and discover why it’s the perfect choice for serious athletes and fitness enthusiasts.

Andarine (S-4): 50 mg

At the core of this supplement is Andarine, included at 50 mg per serving. Andarine, also known as S-4, is a selective androgen receptor modulator (SARM) known for its ability to promote significant muscle growth and strength without the typical androgenic side effects. By selectively binding to androgen receptors in muscle and bone tissue, Andarine enhances protein synthesis and nitrogen retention, which are crucial for muscle development and recovery. Experience the unparalleled muscle-building and strength-enhancing benefits of Andarine and take your performance to new heights.

N-Acetyl L-Cysteine (NAC): 300 mg

N-Acetyl L-Cysteine, or NAC, is included at 300 mg per serving to support overall health and enhance recovery. NAC is a precursor to glutathione, one of the body’s most powerful antioxidants. By boosting glutathione levels, NAC helps protect cells from oxidative stress and enhances recovery. This compound also supports liver health and detoxification, ensuring optimal metabolic function. Enjoy the benefits of improved recovery, reduced fatigue, and enhanced well-being with the antioxidant power of NAC.

Milk Thistle Extract: 200 mg

Milk Thistle Extract is another key ingredient in Andarine, included at 200 mg per serving. Milk Thistle is renowned for its liver-protective properties, thanks to its active compound, silymarin. By promoting liver health and detoxification, Milk Thistle ensures that your body can efficiently process and eliminate toxins, enhancing overall metabolic function. Experience the comprehensive liver support and improved recovery provided by Milk Thistle Extract.

Alpha Lipoic Acid (ALA): 100 mg

Alpha Lipoic Acid, or ALA, is included at 100 mg per serving to provide additional antioxidant support. ALA is a versatile antioxidant that helps protect cells from oxidative damage and supports overall cellular health. This compound also plays a role in regenerating other antioxidants, such as glutathione and vitamins C and E, enhancing their effectiveness. ALA supports metabolic health and recovery by reducing oxidative stress and promoting efficient energy production. Enjoy the comprehensive antioxidant support of ALA for optimal recovery and overall well-being.

Rhodiola Rosea Extract: 100 mg

Rhodiola Rosea Extract is included at 100 mg per serving to enhance endurance and reduce fatigue. Rhodiola is an adaptogen known for its ability to improve physical performance and mental clarity. By reducing the effects of physical and mental stress, Rhodiola helps you maintain peak performance during intense workouts. Experience increased stamina, reduced fatigue, and enhanced overall performance with the adaptogenic benefits of Rhodiola Rosea Extract.

Why Choose Andarine (S-4) by Magnus Pharmaceuticals?

Andarine by Magnus Pharmaceuticals is more than just a muscle-building supplement; it’s a comprehensive solution for achieving your fitness goals. Each ingredient is meticulously selected and dosed to provide maximum benefits, ensuring you get the most out of every serving. Whether you’re a seasoned bodybuilder or just starting your fitness journey, Andarine is designed to help you succeed.

Scientifically Formulated for Maximum Muscle Growth

The ingredients in Andarine are supported by scientific research, ensuring you’re getting a product that’s both safe and effective. Magnus Pharmaceuticals is committed to quality and transparency, providing you with a supplement you can trust. With Andarine, you’re not just taking a supplement; you’re investing in a scientifically formulated product that delivers real results.

Achieve Rapid Muscle Growth and Strength

Andarine is specifically formulated to support rapid muscle growth and strength. The combination of Andarine, NAC, Milk Thistle, ALA, and Rhodiola works synergistically to enhance protein synthesis, promote lean muscle mass, and increase strength. This means you can train harder, recover faster, and see results quicker. Experience the muscle-building and strength-enhancing benefits of Andarine.

Support Overall Health and Well-Being

Andarine doesn’t just focus on muscle growth; it also supports your overall health and well-being. With the inclusion of powerful antioxidants and adaptogens, you can enjoy better nutrient absorption, reduced oxidative stress, and overall improved health. Take your fitness and health to the next level with a supplement that cares about your overall well-being.

Unleash Your Full Potential with Andarine

Don’t settle for ordinary results. Elevate your fitness journey with Andarine (S-4) by Magnus Pharmaceuticals and experience the transformative power of this innovative supplement. Whether you’re aiming for increased muscle gains, improved strength, or better overall performance, Andarine is your key to success. Get your bottle today and start your journey towards a stronger, more muscular, and healthier you. Unleash your full potential and achieve the physique of your dreams with Andarine.

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Intensive Lightning Serum | Clear, and Lightning - Permanence Skin Aka

Permanence Skincare introduces the Illuminate S-acetyl Vitamin C Combo, a powerful skin lightening aid that works from within. Our advanced formula combines S-acetyl L-glutathione, reduced glutathione, N-acetyl L-cysteine, and liposomal vitamin C to provide maximum bioavailability and effectiveness.

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Deciphering the mechanism of p53-mediated ferroptosis

Background of p53

It is well known that p53 is a tumor suppressor gene and essential for regulating DNA repair and cell division. Since its discovery in 1979, p53 gene has been a hot topic in molecular biology and oncology. According to Dolgin, E. et al.’s literature published in Nature, TP53 becomes the most popular human genome in the list of most studied genes in PubMed database[1]. The TP53 gene provides instructions for making a p53 protein.

According to integrated cancer genomic and epidemiological data analyses, TP53 is the most commonly mutated gene (35%) among mutated driver genes in human cancers[2](Figure 1), it is also the most studied gene in the human genome based on PubMed database. TP53 is located on the short arm of human chromosome 17 and encodes the p53 tumor suppressor protein.

The p53 protein is often referred to as the “Guardian of the Genome”. The main biological function of the p53 protein is the protection of the DNA integrity of the cell.

Figure 1: Left, List of most studied genes in the PubMed database as of 2017

[3]

Right, Proportion of epidemiologically weighted gene mutations in important genomes in the cancer patient population

[2]

In response to intrinsic and extrinsic stress signals, the p53 protein is activated by a variety of post-translational modifications including phosphorylation, acetylation, methylation, ubiquitination, or SUMOylating, etc. These modifications at key sites allow p53 protein to become stabilized, oligomerize as a tetramer, interact with cofactors, bind to the p53RE, execute the transcription of the target genes in a tightly controlled and context dependent manner [Figure 2]. In recent years it was found that p53 plays roles in the regulation of ferroptosis. In this article, the connection between p53 and ferroptosis will be explored.

Figure 2. Central role of p53 protein as a tumor suppressor

[4]

Ferroptosis is a novel form of regulated cell death. The morphological features of ferroptosis include shrunk mitochondria with condensed mitochondrial membrane densities, reduction or vanishing of mitochondria crista, and rupture of outer mitochondrial membrane. The p53 (especially acetylation-defective mutant p53, p533KR) positively regulates ferroptosis by inhibiting expression of SLC7A11 (a specific light-chain subunit of the cysteine/glutamate antiporter).

SLC7A11 is a subunit of System Xc-, which is responsible for maintaining redox homeostasis by importing cystine. After transported into cells, cystine is quickly reduced to cysteine, a critical precursor for glutathione and subsequent reduced glutathione (GSH). GSH biosynthesis is critical to functional activity of membrane lipid repair enzyme GPX4. Inhibiting System Xc- activity by inhibition of SLC7A11 expression leads to decreased uptake of cystine, eventually resulting in impaired antioxidant capability of cells and initiation of ferroptosis [Figure 3]. “Ferroptosis as a p53-mediated activity during tumor suppression”, Jiang et al. reported that p53 inhibits expression of SLC7A11, reduces cystine uptake and induces ferroptosis of cancer cells.

Figure 3: The mechanism of p53 mediated ferroptosis

[6]

.The SLC7A11 gene is a target of p53-mediated transcriptional repression

Jiang, L et al. has demonstrated in the "Ferroptosis as a p53-mediated Activity during Tumour Suppression" published in Nature in 2015 demonstrates that p53 supposes SLC7A11 (a key component of the cystine/glutamate antitransporter) to inhibit cystine uptake and sensitize cells to ferroptosis[7].

By microarray analysis of Tetracycline -controlled (tet-on) p53 induced and non-induced cells, SLC7A11 was identified as a novel p53 target gene. Western blot showed that p53 activation significantly reduced SLC7A11 protein levels [Figure 4a]. While in U2OS cells under p53-knockdown conditions treated Nutlin-3 (a p53-MDM2 inhibitor), downregulation of SLC7A11 was abrogated. These data suggest that SLC7A11 gene is a target of p53-mediated transcriptional repression.

The acetylation defective mutant p533KR cells that fails to induce cell cycle arrest, senescence and apoptosis maintain the ability to regulate SLC7A11 expression and induce ferroptosis. Tet-on p533KR inducible H1299 cells were resistant to erastin-mediated ferroptosis in the absence of p533KR induction, while significant cell death was observed upon p533KR induction together with Erastin treatment. But SLC7A11overexpression abrogated p533KR induced ferroptosis [Figure 4c]. In xenograft tumor models implanted with p53-null H1299 cells, tumor size is markedly reduced upon p533KR expression induced by tetracycline, while this tumor suppression effects of p533KR were abrogated by SLC7A11 overexpression[7] [Figure 4d-e].

Figure 4. SLC7A11 regulates p53-mediated ferroptosis

[7]

a: Western blot of Doxycycline-treated tet-on p53 stable line cells; b: Western blot analysis of Nutlin-treated p53-knockdown U2OS cells; c-d: Ferroptosis in Tet-on p53

3KR

cells transfected with a control or SLC7A11-overexpressing plasmid and xenograft tumor weight of cells.

In addition, it was found that high levels of reactive oxygen species (ROS) can trigger p53-mediated ferroptosis. As shown in Figure 5a, no significant cell death was observed in p533KR induction alone or in ROS activator treatment; whereas the p533KR and ROS group induced substantial cell death, which was rescued by overexpression of SLC7A11 (Figure 5b)[7].

Figure 5. Effects of high levels of ROS on p53-mediated ferroptosis

[7]

a-b: Cell death of Tet-on p53

3KR

cells treated with tetracycline and ROS as control or transfected with SLC7A11-overexpressing plasmid;ALOX12 is essential for the p53-mediated ferroptosis pathway

In a follow-up study, Chu B. et al. reported that ALOX12-mediated, ACSL4-independent ferroptosis pathway is critical for p53-dependent tumor suppression[8]. The ALOX12 gene is located on human chromosome 17p13.1, a labile site for monoallelic deletions in human cancers.

ALOX12 was found to be essential for p53-mediated ferroptosis under ROS stress. ALOX12 depletion had no apparent effect on p53 levels or the expression of its transcriptional targets such as SLC7A11, Mdm2, and p21, but it rescued p53-mediated ferroptosis (Figure 6a-b)[8].

Next, it was found that p53-mediated ferroptosis under ROS stress was regulated independently of GPX4. As shown in Figure 6c, high levels of endogenous lipid peroxidation could be detected in GPX4-knockout cells, whereas lipid peroxidation levels were significantly reduced after ectopic expression of GPX4. At the same time, RSL-3 (GPX4 inhibitor) could abrogate the reducing effect of GPX4 on lipid peroxidation, while the activation of p53 had no effect on it[8].

Then, the effect of ALOX12 on p53-mediated tumor growth inhibition was investigated. Tetracycline-induced p533KR expression significantly reduced tumor cell growth. Moreover, ALOX12 knockdown ablated the tumor suppressive effect of p533KR [Figure 6c-d]. These data suggested that ALOX12 is critical for the tumor cell growth inhibitory activity of p53[8].

Figure 6. The role of ALOX12 in p53-mediated ferroptosis under ROS stress

[8]

a: Western blot analysis of U2OS cells; b: U2OS cell death after treatment with different drugs; c: Changes in cellular lipid peroxidation levels; d: Xenograft tumors in H1299 Tet-on p533KR and ALOX12 knockout mice.iPLA2β is a key regulator of the p53-mediated ferroptosis pathway

In June 2022, Chen Du et al. reporteda mechanism in an article "iPLA2β-mediated lipid detoxification controls p53-driven ferroptosis independent of GPX4" in Nature CommunicationsIn this proposed mechanism iPLA2β is a key regulator of p53 activation-induced ferroptosis under high ROS stress conditions and p53 induces ferroptosis in a GPX4-independent manner[9][Figure 7].

Figure 7. Model for the role of ALOX12 and iPLA2β in regulating p53-mediated ferroptosis

[9]

The p53 levels were not affected by ACSL4 and GPX4, in the ACSL4/GPX4 double knockout (ACSL4

-/-

/GPX4

-/-

) human osteosarcoma cell line U2OS. At the same time, p53-mediated transcriptional activation of p21 or repression of SLC7A11 remained unchanged (Fig. 8a). However, when ACSL4

-/-

/GPX4

-/-

cells were exposed to TBH and Nutlin, ferroptosis cell death apparently occurred, which was specifically blocked by ferroptosis inhibitors (Fig. 8b).

Figure 8. p53 mediates ferroptosis in a GPX4-independent manner under ROS stimulation

[9]

a: Effect of Nutlin on p53 protein in U2OS cells; b-d: The effects of cell death influenced by TBH, Nutlin, Ferr-1, Lipro-1, 3-MA, Necrostatin-1, Z-VAD-FMK on WT,ACSL4

-/-

, GPX4

-/-

and U2OS cellsConclusion:The tumor suppressor gene

TP53

is the most studied gene in cancer research. Ferroptosis is a novel form of regulated cell death that has sparked a research frenzy since its discovery. The discovery of connection between p53 and ferroptosis paves a new way for the development of p53-related drugs for cancer treatment.

Related products

Nutlin-3

A potent p53-MDM2 inhibitor with Ki of 90 nM.

Idasanutlin

A potent and selective MDM2 antagonist that inhibits p53-MDM2 binding with IC50 of 6 nM.

Pifithrin-α hydrobromide

A p53 inhibitor that blocks its transcriptional activity and prevents apoptosis; an agonist of aryl hydrocarbon receptor (AhR).

Erastin

A ferroptosis inducer that binds and inhibits voltage-dependent anion channels (VDAC2/VDAC3).

RSL3

An inhibitor of glutathione peroxidase 4 (GPX4) (ferroptosis agonist) that reduces GPX4 expression. .

Ferrostatin-1

A selective ferroptosis inhibitor; antioxidant.

References

[1]. Liz J Hernández Borrero 1, Wafik S El-Deiry, et al. Tumor suppressor p53: Biology, signaling pathways, and therapeutic targeting. Biochim Biophys Acta Rev Cancer. 2021 Aug;1876(1):188556.

[2]. Gaurav Mendiratta, et al. Cancer gene mutation frequencies for the U.S. population. Nat Commun. 2021 Oct 13;12(1):5961

[3]. Elie Dolgin, et al. The most popular genes in the human genome. Nature. 2017 Nov 23;551(7681):427-431.

[4]. Sandra L Harris, et al. The p53 pathway: positive and negative feedback loops. Oncogene. 2005 Apr 18;24(17):2899-908.

[5]. Ou M, et al. Role and mechanism of ferroptosis in neurological diseases. Mol Metab. 2022 Jul;61:101502.

[6]. Y Xie, R Kang, D Tang et al. Ferroptosis: process and function. Cell Death Differ. 2016 Mar;23(3):369-79.

[7]. Le Jiang, Wei Gu, et al. Ferroptosis as a p53-mediated activity during tumour suppression. Nature. 2015 Apr 2;520(7545):57-62.

[8]. Bo Chu, Wei Gu, et al. ALOX12 is required for p53-mediated tumour suppression through a distinct ferroptosis pathway. Nat Cell Biol. 2019 May;21(5):579-591.

[9]. Delin Chen, Wei Gu, et al. iPLA2β-mediated lipid detoxification controls p53-driven ferroptosis independent of GPX4. Nat Commun. 2021 Jun 15;12(1):3644.

[juniperpublishers-toxicology]

Fulminant hepatic failure induced by antipsychotic drugs (a case report)

Introduction

Fulminant hepatitis is a rare condition but has a very poor prognosis in the absence of liver transplantation. It is important to identify the cause as soon as possible to start the etiological treatment, which may be drug poisoning, viral hepatitis, or alcoholic ... [1-3]. N-acetylcysteine (NAC), a glutathione precursor, was first used as a treatment for paracetamol overdose in 1979. Since then, it has been firmly established as an effective and safe treatment for paracetamol induced IHC prevention. NAC has also been shown to be effective outside paracetamol intoxication. It has been evaluated as an option for acute IHC other than paracetamol in adults and children. In a randomized clinical trial comparing NAC with placebo in adults with paracetamol-free IHC, NAC was associated with a marked improvement in survival without liver transplantation [4]. NAC has also been evaluated for non-hepatic clinical conditions, these indications include its use in lung diseases (COPD and pulmonary fibrosis), in the prevention of contrast-induced nephrotoxicity and for the treatment of certain cardiac diseases [3,5]. In this article, we report the case of a neuroleptic overdose in a 16-year-old who has rapidly progressed to fulminant hepatitis. The oral administration of N-acetylcysteine has allowed a dramatic improvement [3].

Observation

A 16-year-old man consulted at the emergency reception service (j1) for asthenia, disabling diffuse myalgia and uncontrollable vomiting, in the context of cutaneous-mucous jaundice, which had appeared for 4 days. Her antecedents included herpetic keratitis since the age of 3 years and chronic epigastralgia for 4 years. In the emergency department, the clinical examination found a sleepy, sleepy patient, a conjunctival subitem, muscle pain with manual pressure. The temperature was 37.8°C, and blood glucose was 2.2mmol/l. The blood pressure was 85/38 mmHg, the heart rate was 104 beats per minute and 95% saturation in the air. The biochemical assessment was very disturbed, with: an inflammatory syndrome (C-reactive protein at 150 mg/L, fibrinogen at 6.6g/L), renal insufficiency (urea at 14.4mmol/L, creatinine at 159 , 12mmol/L), cytolysis (ASAT: 10454 IU/L, ALA at 4408 IU/L), cholestasis (conjugated bilirubinemia at 151mmol/L, gamma GT at 489 IU / L, PAL at 657 IU/L ) and a disturbance of its hemostasis (TP <15%, a TCA at 96.4 s and a very collapsed factor V). The hemogram showed the following: white blood cells at 9210mm-3, platelets at 159 000mm-3 and hemoglobin at 11.2g/dl.

On the diagnosis side

The patient was admitted to intensive care (1st day). Etiologically, an infectious hypothesis has been ruled out by the negativity of his liver serologies (anti-HVA Ab, anti-HBV Ab and HBs antigen and anti-HCV antibodies) as well as the serology of CMV, the abdominal ultrasound was without particularities, blood ceruloplasmin level was normal, anti-smooth muscle and antimitochondrial antibodies were achieved returning normal. The preferred toxic hypothesis was a neuroleptic overdose because the interview reported a prescription of 3 different neuroleptics, by his doctor for his chronic epigastralgia of psychogenic origin (Olanzapine, Mainspring and Metoclopramide). Supported: Symptomatic treatment consisted of stopping neuroleptics, infusion of fresh frozen plasma, vitamin K, laxatives and ciprofloxacin were initiated associated with administration of N-acetylcysteine with a dose of oral load of 140mg/kg followed by a dose of 70mg/kg/day maintenance for 48 hours.

Evolution

The evolution was quickly favorable. Hyper-bilirubinemia was divided by five in three days, the state of consciousness improved rapidly with appearance of an asterixis, the correction of the hemostasis disorder was more progressive with normalization towards the 4th day (Figure 1), a dramatic improvement in hepatic transaminases was observed as early as the second day (Figure 2). The patient left the intensive care unit to the gastric department on day 6. The symptomatic treatment was continued until day 10, the PBH was performed on day 11 without abnormality then he left the hospital on day 17.

Discussion

IHA is defined as a sudden failure of liver function in a patient with no history of liver disease. The cardinal signs of hepatic failure include coagulopathies and hepatic encephalopathy of any grade in the context of acute liver injury [4]. Currently, there is no scientifically proven beneficial treatment in the treatment of IHC, apart from liver transplantation Lee [5]. More than 1000 drugs have been listed as being responsible of hepatic side effects; 16% of these agents were neuropsychiatric drugs. Antidepressant drugs (tricyclic agents or SSRI), mood stabilizing agents and neuroleptic drugs have been implicated in biological or/and clinical hepatotoxicity. For these reasons, some psychotropic agents have been withdrawn of the pharmaceutical, On the contrary, in case of clinical hepatotoxicity, challenge or maintenance is absolutely inadvisable. Mechanism of the hepatic troubles: precise mechanisms of the hepatotoxicity remain unclear. Contrary to phenothiazine drugs, no information is available on the respective rule of the agents and their metabolites. Hypersensitivity syndrome or eosinophilia has been reported, suggesting a possible immuno-allergic mechanism. Presence of risk factors: risk factors have been retrieved, in some observations, like high daily dosage, high plasmatic concentration, age, alcoholism, obesity or antecedent of hepatic disorders like Gilbert syndrome. [6] Special care is advisable with these patients. As hepatotoxicity has been observed after surd Osage (or suicide attempt), a hepatic check-up has to be performed in these clinical situations [7]. Co-medication with hepatotoxic drugs may increase the risk as it has been suggested. Acetylcysteine is a precursor of glutathione. It is well known as an antidote for acetaminophen overdose due to its ability to increase glutathione levels, which inactivates the toxic metabolite of acetaminophen [8]. N-acetyl-pbenzoquinone mine. Glutathione is a major antioxidant that can serve as a scavenger for free radicals; therefore, acetylcysteine may increase glutathione stock during periods of oxidative stress, increase nitric oxide production, which causes vasodilation and therefore tissue oxygenation, and may also have an antiinflammatory effect. by inhibition of pro-inflammatory factors (TNF alfa and IL8) [9,10]. The majority of studies evaluated the use of NAC in acute IHC secondary to acetaminophen poisoning. There is little research on the use of NAC in IHC secondary to other causes. Hu [8]. evaluated the efficacy of NAC in patients with non-acetaminophen-overdosed IHC (safety and efficacy of NAC in patients with ALF not caused by acetaminophen overdose), in a meta-analysis, which consisted of analyzing four assays prospective clinical trials evaluating NAC versus placebo in the treatment of non-acetaminophen-induced IHC[3].

Conclusion

NAC is a beneficial treatment in the context of nonparacetamol induced IHC, it can prolong the survival of patients with or without liver transplantation and survival after transplantation, but it cannot improve overall survival. Therefore, due to the lack of available scientific evidence, current data is unable to conclusively determine the role of NAC in patients with IHC without paracetamol. Thus, they are unable to make recommendations for clinical practice.

[skin-care1-blog1]

Best s-acetyl l-glutathione

A mother everything being equal and a safe framework promoter, Best s-acetyl l-glutathione causes our body to remain solid as shown by a few examinations. Glutathione not just shields us from particular sorts of maladies yet it likewise treats intellectual issues, from mental imbalance to Alzheimer's infection, and a wide exhibit of other medical issues. Truth be told, keeping up elevated levels of glutathione is basic to interminable malady the board and recuperation.

 A fundamental aspect of the detoxification cycle, Best s-acetyl l-glutathione is basically found in the liver which is the primary organ answerable for detoxification however it likewise works in the tissues and organs all through the body. Glutathione ousts poisons in a structure that can be discharged through the bile and stool, and it reuses different cancer prevention agents including nutrients C and E. Past detoxification, glutathione assumes a critical function in vitality digestion. This basic particle shields cells and mitochondria from free extreme harm. Mitochondria are the forces to be reckoned with in cells that are answerable for vitality creation, and by keeping it liberated from oxidative harm, permits the cell to accomplish top execution along these lines advancing ideal wellbeing and expanded vitality.

 Our body delivers its own glutathione; be that as it may, its sum decreases with terrible eating routine, stress, disease and presentation to poisons, contamination, and radiation. It likewise begins to drain at 45 years old. Examination shows that solid youngsters have elevated levels of glutathione while undesirable older have low degrees of this cell reinforcement, and it is even lower among debilitated and hospitalized old. With low degrees of glutathione in the body, we become more inclined to contamination and sicknesses as we do not have the capacity to adequately detoxify. This likewise makes harm the liver which further subverts the detoxification cycle.

 To keep up ideal mental and physical capacity, it is basic to keep elevated levels of glutathione even before we arrive at the age of 45 as we are presently more presented to a few natural factors that accelerate the exhaustion of glutathione in our body. Taking glutathione supplements alongside devouring Best s-acetyl l-glutathione boosting food and exercise is a decent choice.

 Glutathione might be taken orally or through inward breath or infusion. A few oral glutathione supplements are accessible available however there are inquiries with regards to their bioavailability. When glutathione arrives at the stomach, it is separated and gets inadequate. A more absorbable and profoundly stable type of glutathione, S-Acetyl Glutathione, is presently accessible.

 It is difficult to exaggerate the significance of glutathione, key functions of which are summed up. It assumes a pivotal function in protecting cell macromolecules from endogenous and exogenous receptive oxygen and nitrogen species. While it legitimately extinguishes some free extremists, of maybe more noteworthy significance is that it manages the reasons for oxidative pressure, for example, mercury and POPs.

 Glutathione is engaged with the detoxification of both xenobiotic and endogenous mixes. It encourages discharge from cells (Hg), encourages discharge from body (POPs, Hg) and straightforwardly kills (POPs, numerous oxidative synthetic substances). Glutathione encourages the plasma film transport of poisons by at any rate 4 distinct instruments, the most significant of which is arrangement of glutathione S-forms. Low degrees of glutathione and additionally transferase action are likewise connected with ceaseless presentation to concoction poisons and liquor, cadmium introduction, AIDS/HIV, macular degeneration, Parkinson's illness, and other neurodegenerative issues.

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Metformin Reduces the Extent of Varicocele-Induced Damage in Testicular Tissue

Authored by: Erkan Erdem*

Introduction

Varicocele is an abnormal vascular dilatation of pampiniform plexus, commonly developing at puberty. Although underlying mechanisms remain poorly understood genetic background, anatomical aberrations, incompetence of venous valves, difference between the drainage of left and right testicular veins were suggested in the etiology [1]. As left spermatic vein being longer than the right vein, it is more commonly incurred to increased hydrostatic pressure and dilatation. Compression of the left renal vein between the aorta and the superior mesenteric artery may also contribute to the disturbed intravenous pressure [2].

The prevalence of varicocele varies between 15-20 % in general population and 30-40% in infertile men, and 11-19% of adolescents [3-6]. It was reported that varicocele is a progressive disease and early diagnosis and treatment in youth may enhance fertility potential [7]. Several contributing factors in the pathophysiology of varicocele have been proposed such as higher temperature of testis, the disorder of neuroendocrine system, autoimmunity, accumulation of renal and adrenal metabolites, genetic and epigenetic factors, hypoxia and oxidative stress [8-10].

Varicocele represents a chronic process within the testicle, which is linked to increased reactive oxygen species (ROS) beyond physiologic limits and, subsequently, disrupting sperm membrane fluidity, causing DNA damage and necrosis [11]. Moreover, superoxide dismutase 1, glutathione S-transferase M1 and T1 which are counteracting free superoxide radicals in cells have been reported to be decreased in men with varicocele, that may be important on disturbed sperm parameters [12]. Apoptosis of germ cells was also demonstrated in the pathogenesis of varicocele-related infertility [13]. Clinical findings suggest that surgical repair of varicocele may decrease seminal oxidative stress levels and sperm DNA fragmentation and, thus, may improve sperm quality [14]. Therefore, surgical intervention seems to be a reliable option in the treatment of varicocele-related male infertility, although some controversial reports exist.

Additionally, anti-oxidant medications such as kallikrein, L-carnitine with L-acetyl carnitine, pentoxifylline, coenzyme Q10 have been used to improve the milieu in the testis in men with varicocele [15]. Metformin is a major therapeutic agent in the treatment of type 2 diabetes mellitus as an insulin sensitizer, which decreases hepatic glucose output and increases peripheral glucose uptake. Although its action was not fully elucidated, metformin attenuated intracellular reactive oxygen species and apoptosis in aortic endothelial cells, myocardium, renal tubular cells and testicular cells [16-20].

Aim

Potential effects of metformin on varicocele-induced testicular damage have not been studied in neither humans nor in animal models. Thus, we investigated the impact of metformin on spermatogenesis, testicular integrity, and apoptotic activity in the testis of adolescent rats with experimentally-induced varicocele.

Materials and Methods

Thirty-six male adolescent Wistar rats (6-week-old) were randomly and equally divided into six experimental groups. Surgical procedures were carried out under anesthesia with intraperitoneal injection of ketamine (50 mg/kg). The experimental groups were as follows:

• (C) Control group; no surgical procedure was performed, and testis was examined after removal.

• (S) Sham group, a midline incision was performed, and testis was examined 8 weeks later.

• (V) Varicocele - only group: Experimental varicocele was induced by partial ligation of left renal vein with

Silk suture at the area medial to the insertion of the adrenal and spermatic vein into renal vein as described previously [21].

• (V+M) Varicocele + metformin group: All rats were treated with metformin (300 mg/kg per day by oral gavages) for 8 weeks following induced varicocele.

• (V/E) Varicocele + varicocelectomy group: Varicocelectomy was performed 4 weeks and the examination of the testis 8 weeks after the induction of varicocele. No medication was used.

• (V/E+M) Varicocele + varicocelectomy + metformin group: Varicocelectomy was performed 4 weeks after the induced varicocele. Metformin treatment (300 mg/kg per day by oral gavages) was initiated after the induction of varicocele and continued for 8 weeks. Left testes were examined 8 weeks after the induction of varicocele in all varicocele - induced groups. As maximum apoptotic activity initiates approximately 28 days after the induction of varicocele the procedure of varicocelectomy was performed 4 weeks after the formation of varicocele [22].

Histologic preparation and evaluation

The testicular tissue was fixed in Bouin’s solution (75% picric acid, 5% glacial acetic acid, and 25% formaldehyde) and embedded in paraffin blocks. Sections (5 μm) were formed, deparaffinized, and stained with hematoxylin and eosin. Spermatogenesis was examined in each group using Johnsen’s score (a score of 1-10 was assigned to each tubule regarding epithelial maturation) as described previously [23]. Sections were examined in a random order under a standard light microscope with 10x and 40x magnification by a blinded histologist; unaware of which group each rat belonged to. Histological grading was done by examining approximately 80 randomly selected seminiferous tubules per rat. Thus, a total of approximately 480 seminiferous tubules were scored for each group.

Histomorphometry analysis

A total of 103 randomly selected seminiferous tubules stained with hematoxylin-eosin were analyzed in each group. The presence of round spermatid stage (RSS) and primary spermatocyte stages (PSS) were assessed as described previously and compared among the groups [24].

Immunohistochemical staining for cleaved caspase-3 and ImageJ analysis

Cleaved caspase-3 was used for immunohistochemical staining. Testicular tissue samples were immediately fixed in 10% neutral-buffered formalin, embedded in paraffin, and sectioned (5 μm). Sections were deparaffinized and blocked for endogenous peroxidase activity with methanol containing 3% H2O2 for 10 m. Ultra V Block (Lab vision, Freemont, CA) for 7 m at room temperature. Cleaved Caspase-3 (#9664, Cell Signaling, U.S.) was applied at a dilution of 1: 500 and incubated overnight at +4 °C in a humidified chamber for nonspecific binding. The sections were washed in phosphate-buffered saline (PBS) and incubated with biotinylated horse anti-rabbit IgG (3 mg/mL; Vector, Burlingame, CA) at a 1: 500 dilution for 1 h at room temperature.

Antibodies were detected using a VECTASTAIN avidinbiotin complex (Vector PK 4000) for 30 m at room temperature. Antibody complexes were visualized after incubation with 3,3’-diaminobenzidine tetrahydrochloride (DAB, Bio-Genex, San Ramon, CA.) and were mounted under glass coverslips in Entellan (Merck) and then evaluated under a light microscope. Immunohistochemical staining for cleaved caspase-3 was analyzed by counting 100 seminiferous tubule cross-sections in each group and expressed as the apoptotic index. In each photomicrograph, the following parameter was measured with ImageJ software: expression levels of cleaved-caspase-3 in both groups at round spermatid stage (RSS) of testes. Each of this parameter was measured 3 times for each image and the average of the 9 measurements of each sample was used for the statistical analysis. Histopathological features examined in rats with normal testis and with sham, varicocele, varicocele+ metformin in a subjective scoring (0 - not present; 1 - low grade; 2 - moderate grade; 3 - high grade; 4 - very high grade).

Statistical analysis

Histopathological findings (Johnsen’s score) were assessed by nonparametric Kruskal-Wallis test, and the mean Johnsen’s score was used in the comparison of the groups. Multiple comparisons were made using Tukey’s procedure. p<0.05 was considered statistically significant. Analysis of variance was used for statistical analysis of the apoptotic index among the groups.

Results

Assessment of spermatogenesis

Johnsen’s score was significantly lower in V group (4.14±1.25) compared to C group (9.1±0.3) or S group (9.0 ± 0.2) groups (p<0.05). V+M group had significantly higher score (6.9±0.6) than V group (p<0.05). V/E group and V/E+M group had similar Johnsen scores (8.9 ± 1.02 and 9.2 ± 0.6). These findings suggest that the administration of metformin resulted in 40.6% of improvement in spermatogenesis in rats with varicocele. However, this favorable effect was not observed when metformin was used along with varicocelectomy.

Histological and morphological changes in seminiferous tubules

Histological and morphological changes in the testes of rats were compared via hematoxylin and eosin staining and degenerated tubules (DT) were only detected in V and V+ M groups, not in C, S, V/E and V/E+M groups (Figure 1). Visual assessment of the disorganized seminiferous tubules further supported these findings as seen in Figure 2. Seminiferous tubule degeneration scores were used for quantification of data (Figure 2b). V group had significantly higher scores of RSS and PSS compared to C and S group (2.6±0.8 and 3.7±0.4; 0.2±0.4 and 0.2±0.4; 0.9±0.6 and 0.6±0.7, respectively) (p<0.05). V/E group had significantly lower RSS (0.7±0.8) and PSS (0.8±0.7) scores than V group (p<0.05). V+M group had significantly lower RSS and PSS scores (1.8±0.7 and 2.6±0.7, p<0.05) in comparison to V group, implicating beneficial effects of metformin in rats with varicocele. When compared to V/E group, V/E+M group did not exhibit any difference in RSS (0.6±0.6) and PSS (1.4±0.5) scores, suggesting the absence of additive positive effect of metformin in varicocelectomies rats.

Apoptotic activity

Apoptotic activity was assessed by using cleaved caspase 3 expressions levels, staining of cleved caspase 3 positive seminiferous tubules were shown in Figure 3a. Cleaved caspase 3 expressions were significantly higher in V group (3.5 ± 0.5) compared to C (0) and S (0.2 ± 0.4) groups. V+M group had significantly lower cleaved caspase 3 level (3.0 ± 0.7) than V group. V/E group had lower cleaved caspase-3 expression levels (1.0 ± 0.7) compared to V group. Treatment of varicoceleectomy rats with metformin (V/E+M) did not further reduce apoptotic activity in the seminiferous tubules (1.75 ± 0.43) when compared to the varicocelectomy group (V/E) (Figure 3b).

Discussion and Conclusion

The present study demonstrates that metformin can reduce the extent of testicular damage in rats with varicocele, although having no effect in rats following varicocelectomy Spermatogenesis, seminiferous tubule integrity and the degree of apoptosis were improved using metformin in the presence of varicocele although it was not as remarkable as what was obtained through varicocelectomy. A review of the literature revealed that the impact of metformin on varicocele was not investigated in humans or animal models until now.

Although it is a commonly identified abnormality not all men with varicocele present with infertility. Some intrinsic factors may render some men to become susceptible to varicocele, thus, the best candidates who benefit from varicocelectomy yet to be clarified. Since oxidative stress was shown to be important in the pathophysiology of varicocele some agents have been used to improve the milieu in the testis [1]. A number of anti-oxidant medications have been studied to relieve detrimental effects of varicocele in the testis [25]. These agents have been used either alone or as an adjuvant therapy with surgery. However, surgery remains the treatment of choice and there exists insufficient data to recommend medical therapy in men with varicocele. Barekat et al. [26] reported that administration of an antioxidant agent N-acetyl cysytein as an adjunct therapy improved semen quality following varicocelectomy [26]. Tek et al. [21] demonstrated that vascular endothelial growth factor decreased apoptosis in varicoceleinduced rats as evidenced by diminished caspase-3 positive cells [21]. Both studies showed the benefit of these as adjunct therapy following varicocelectomy. However, in the present study metformin did not enhance the effect of varicocelectomy.

Minutoli et al. [13] demonstrated that neuronal apoptosis inhibin factor and surviving expressions were significantly reduced following varicocele induction and polydeoxyribonucleotide, an agonist of adenosine A2A receptor, administration restored testicular function [13]. Several other studies detected increased germ cell apoptosis in rats with varicocele [21,22,27]. However, in another study, apoptosis was found to be decreased in germ cells in the testes of infertile men with varicocele as compared with normal men [28]. It was speculated that the fixation of testis in formaldehyde might have played a role in the different result. In the present study, cleaved caspase 3 expression was used to assess apoptotic activity and it was found that metformin reduced apoptotic activity in rats with varicocele, whereas no additional effect was observed when metformin was administered after varicocelectomy.

Metformin is commonly used in type 2 diabetes mellitus and polycystic ovarian disease as an insulin sensitizer [29]. Also, it is present in various tissues including myocardium, liver, pancreas, thyroid, adipose tissue, hypothalamus, pituitary, and male and female gonads [19,30,31]. It has been reported that metformin is mainly transported into cells by organic cation transporters as passive diffusion is limited [32]. Although the mechanism of action is not yet fully elucidated recent studies suggested that metformin acts through AMP-activated protein kinase (AMPK) pathway, inhibits the activity of the respiratory electron transport chain in mitochondria, induces epigenetic modifications which in part may explain long term effects and decreases oxidative stress and apoptotic activity [16,19, 33-35].

Male reproductive system utilizes all these metabolic pathways and is prone to be affected by metformin administration [20,36,37]. Metformin was found to stimulate lactate production which is important in the development of germ cells and show an anti-apoptotic effect in rat Sertoli cells [38]. It was also reported that metformin reduced the apoptotic cells and caspase-3 level in rat testis [20]. The findings of the present study are consistent with previous studies that metformin reduced apoptosis in testis with varicocele. Yan et al. [37] reported that metformin improved the semen parameters related to its effects on weight loss, increased testicular weight and reduced testicular cell apoptosis [37]. On the other hand, Tartarin et al. [36] reported metformin at concentration 10 times higher than therapeutic levels decreased testosterone secretion and the number of Sertoli cells in rats when it was administered during pregnancy [36]. Faure et al. [39] reduction in testicular weight and testosterone level were observed in 6-week-old chickens treated with metformin for 3 weeks [39].

Several groups demonstrated that post-operative administration of metformin can exert protective effects in male reproductive function in rat models [40]. Bosman et al. [41] demonstrated that infertile hyperinsulinaemic men could benefit from metformin treatment in combination with an enriched antioxidant diet [41]. Besides, metformin was reported to act as a protective compound when used in the media for cryopreservation of spermatozoa [30]. In conclusion, metformin reduces detrimental effects of varicocele, although no additional benefit is expected following varicocelectomy. Further studies are required to apply metformin for this indication in humans.

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Livon Alpha Lipoic Acid Supplement online

Alpha Lipoic Acid (ALA) resembles a character entertainer; it's a profoundly flexible cancer prevention agent that is found in about everything, yet you may not realize it by name. What's more, when you realize what alpha lipoic corrosive does, this cancer prevention agent can get everyone's attention. Before buying Livon Alpha Lipoic Acid Supplement online you need to understand its functions and need.

Alpha Lipoic Acid passes by a few names and shortenings, including ALA, Lipoic Acid, LA, Thioctic Acid, Lipoate, and α-lipoic corrosive. Albeit less usually utilized, Alpha Lipoic Acid may likewise be alluded to as 6,8-thioctic corrosive, 6,8-dithioctane corrosive, 1,2-dithiol-3-valeric corrosive, and DHLA.

Its numerous nom de plumes surely don't help its name acknowledgment, yet perhaps these alpha lipoic corrosive advantages will.

ALA = Energy

Cell vitality is the power behind each and every activity inside the human body, including muscle development, age of new cells, wound mending, and notwithstanding thinking. You are utilizing significant cell vitality at the present time, just by perusing this article.

The body's supply of cell vitality begins in the mitochondria of the cells. There are a huge number of mitochondria in most eukaryotic (cells with cores) inside the body, and they are always making vitality through a procedure known as the Krebs Cycle. ALA is a significant cofactor to two key enzymatic responses inside this Cycle. Basically, without ALA, cell vitality is beyond the realm of imagination. What's more, without cell vitality, life is beyond the realm of imagination.

ALA and Healthy Blood Sugar Levels

Apparently one of the most significant Alpha Lipoic Acid advantages is its impact on insulin, and the body's utilization of (glucose). Numerous fake treatment controlled examinations have demonstrated that day by day dosages of 600 mg to 1,800 mg of ALA can keep up solid insulin affectability and the usage of glucose, enabling you to keep up sound glucose levels.

Alpha Lipoic Acid advantages may go above and beyond and help to avoid the complexities that are related with undesirable glucose levels, explicitly intricacies in the vascular framework and kidneys. Late research shows this diminished danger of difficulty originates from ALA's capacity to secure the internal covering of veins (the endothelium) from harm brought about by oxidative pressure.

ALA Is an Important Part of Your Weight-Loss Plan

Consistently, a great many various enhancements, rec center participations, pharmaceutical medications, books, and therapeutic medicines are utilized by individuals attempting to get more fit. In 2012, the yearly income of the USA weight reduction industry was an expected $20 billion.

Alpha Lipoic Acid can't mysteriously make sweet as nutritious as carrots, however it has an impact on how our bodies use sustenance and abundance fat. Late research demonstrated that overweight individuals who took 1,800 mg ALA consistently for 20 weeks lost more weight than subjects who did not take ALA. Everything boils down to cell vitality. By supporting the making of vitality inside the cells, one of the Alpha Lipoic Acid advantages is that it can help animate the body to utilize sustenance particles all the more rapidly and consume abundance calories from fat.

Alpha Lipoic Acid Is a Powerful Antioxidant

Cancer prevention agents secure the body against dangerous free radicals. Cell reinforcements, for example, nutrient C, nutrient E, Glutathione and R-ALA kill free radicals by giving one of their own electrons. So pause, wouldn't the cancer prevention agent become a free radical since it lost an electron? No, these cell reinforcements are steady in either structure. They go about as givers, giving electrons to anticipate cell harm and malady. For the most part, when cell reinforcement kills a free radical, it is lost for eternity. R-ALA has the extraordinary capacity to recover itself, just as different cell reinforcements, for example, nutrient C, so they can keep on pulverizing free radicals. R-ALA is the doctor in the field, guaranteeing its fighters can keep on winning the war against free extreme harm.

Picking the Right Form for Maximal Alpha Lipoic Acid Benefits

ALA can be found in oral enhancements in two structures: the R structure, which is the structure found in nature, or the S structure. The R type of ALA is more bioavailable and naturally dynamic than S-ALA, yet it is costly to deliver and frequently shows strength issues in assembling. This is the reason numerous ALA enhancements contain just the S structure, or a 50/50 blend of S-ALA and R-ALA (additionally alluded to as racemic ALA).

Much of the time, just half of the all out portion of enhancements named as Alpha Lipoic Acid or R/S Lipoic Acid is the R structure. Since R-ALA has as of late turned out to be accessible in a settled organization, most clinical research has been led utilizing intravenous or oral blends of R/S ALA. This is essential to think about when picking the amount ALA to take. For instance, when clinical proof recommends 600 mg of racemic ALA every day can help keep up solid glucose levels, this portion would be proportional to 300 mg of R-ALA.

Liposome typified R-ALA may upgrade the Alpha Lipoic Acid advantages by giving better retention and usage of R-ALA in the body. ALA pills, powders and cases are quickly, yet deficiently assimilated into the blood, and after that immediately utilized by the body or go as waste. With Liposomal Encapsulation Technology, our Lypo-Spheric® R-Alpha Lipoic Acid is typified and shielded from annihilation in the stomach related framework by tiny liposomes. Since liposomes are made of phospholipids (a similar material that makes up your phone film), they are prepared to do going through cell layers and conveying R-ALA legitimately into the cell.

Various investigations have demonstrated that Alpha Lipoic Acid (ALA) builds glucose take-up in cells, implying that you get the sugar you have to work out in your dynamic muscles, not gathering in fat stores on your midsection. Because of this capacity, various fake treatment controlled investigations have demonstrated that day by day dosages of Alpha Lipoic Acid can keep up sound insulin affectability. For what reason is insulin affectability significant when assessing nutrients for muscle development?

Insulin moves glucose out of your blood and into the muscle cells where it's expected to give vitality to move a free weight. In case you're delicate to insulin, as your body is intended to be, the sugars you expend will be utilized for their proposed reason: fuel. On the off chance that you eat an eating regimen with an excess of sugar and prepared sustenance, you send more glucose to the blood than the insulin receptors in the muscle cells can utilize. They treat insulin like the kid who falsely sounded the alarm and quit reacting appropriately, leaving overabundance glucose sitting in the circulatory system for conveyance somewhere else. Furthermore, your waist looks more like a barrel than a six-pack.

Various examinations have affirmed that Alpha Lipoic Acid improves glucose take-up in skeletal muscle. Thus, it bodes well that a recent report found that ingesting ALA alongside creatine and a modest quantity of sucrose expands muscle creatine content. As it were, it gets your creatine supplement where it needs to go to invigorate protein amalgamation fundamental for quality and size increases without devouring as much sugar.

In a recent report, analysts found that enhancing with Alpha Lipoic Acid builds muscle GLUT-4 substance in rodents. Excess 4 is the receptor that transports glucose through the circulatory system to the cells. By expanding the substance of muscle GLUT-4 receptors, it makes sense that the more glucose can arrive at the muscles rather than fat cells.

As Burt Berkson, M.D., Ph.D., and one of the world's premier experts on ALA writes in his book The Alpha Lipoic Acid Breakthrough, "In the cell, glucose is set up for ignition and vitality generation. The readied glucose can't pick up passage into the mitochondrion when there is no alpha lipoic corrosive accessible. At the end of the day, without ALA, fuel can't enter the mitochondrion and no vitality can be created."

Berkson likewise aggregates up what might be the significant advantage for competitors utilizing nutrients for muscle development in enhancing with Alpha Lipoic Acid: "Glucose is the essential glucose. To turn into a phone fuel, it must be separated into two littler atoms called pyruvate. Pyruvate can't be scorched for vitality until it is changed into a compound considered acetyl coenzyme A. Pyruvate can't move toward becoming acetyl coenzyme A without ALA. On the off chance that more ALA is accessible, more acetyl coenzyme An is delivered, and thus, more vitality is created."

Your liver creates enough of it to help with cell digestion and get its cancer prevention agent benefits. Tragically, as Glutathione, your body creates less of it as you age and you need it more. That is the reason wellness experts have been enhancing with it for quite a long time with dosages no higher than 600mg/day.

Alpha Lipoic Acid is anything but difficult to discover in the enhancement walkway. The issue is that the vast majority of the less expensive cases utilize the manufactured (S) adaptation of Alpha Lipoic Acid, which isn't viable in helping our cells process glucose and in this manner not a powerful nutrient for muscle development. Lypo-Spheric® R-ALA utilizes 226mg of the R assortment of Alpha Lipoic Acid that is found in nature.

Taking nutrients for muscle development won't get you tore without the reps. The examination says that in blend with opposition preparing, recuperation, and a muscle-building diet, enhancing with Glutathione, L-Carnitine, and the R type of Alpha Lipoic Acid can enable you to get increasingly out of every rep. Asterveda Healthcare offers each of the three enhancements in liposomal typified structure for most extreme assimilation. They're accessible in advantageous, uni-portion bundles sold in containers as a month's supply, so you can upgrade your muscle-building routine for only a few dollars every day. Asterveda Healthcare is well known for Livon Alpha Lipoic Acid Supplement online.

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CAPTAVIDA IMMUNE + GUT HEALTH 60 CT

Your Immune System is your shield against illness, viruses, and disease. But did you know that 70% of your immune system resides in your Gut? Therefore, Gut health is critical to a healthy immune system. Captavida Immune + Gut Health is a powerfully effective formula that combines five of the most potent immunity and Gut health ingredients in one simple solution; Zinc, Holy Basil, Vitamin D3, Marshmallow Root, and S-Acetyl L-Glutathione. Individually, each of these powerful ingredients offers critical health benefits. But combined, they are even more effective and provide the ultimate defense against the external forces threatening your health every day.

This product does not contain Hemp-Derived Cannabidiol.

This product is manufactured in an FDA Registered and GMP Compliant Facility.

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8 Key Vitamins for Beautiful Skin and Optimal Health

There are many vitamins your skin and your body need to be healthy and vibrant. In this article I will focus on 8 key nutrients.

Your skin is a reflection of your overall health and well-being.

The vitamins and nutrients that will help your skin look it’s best also make the rest of your body work its best. What’s good for the skin is good for the rest of the body and vice versa. If your skin is showing signs of aging, this is more than an issue of personal vanity. External aging and internal aging are intimately related. Poor skin can be a sign of poor health.

So today I want to talk a bit about the intimate relationship between your skin and the rest of the body. Along the way we will cover some steps you can take to turn back the hands of time, reverse the effects of aging, and get that younger, tighter, glowing skin you’ve always dreamed of.

Skin Science 101

Your skin is one of the largest and most important organs in your body. Unfortunately, most of us simply don’t give our skin the support it needs so it can function at its best.

You see, the cells in the outer layer of your skin—the epidermis—divide continuously, which means they need a lot of nutritional support. The deeper layers—the dermis—are made up of the collagen and elastin proteins, which also need plenty of support and are often undernourished by the standard American diet and lifestyle.

Skin aging is a complex biological phenomenon that consists of two independent and biologically distinct processes: intrinsic aging and extrinsic aging.1

Intrinsic aging, as its name suggests, comes from within. It is the type of damage that affects any cell in the body. One of the primary causes are free radicals which cause oxidation (rusting) of cell membranes, DNA, and so on. To combat this type of oxidative damage, it is recommended you eat a plant-based diet rich in natural antioxidants. And, as so many of us are depleted of these natural antioxidants, supplementation can help as well.

Extrinsic aging is aging from without and refers primarily to “photo-aging”: the result of exposure to outdoor elements such as ultraviolet (UV) irradiation. Photo-aged skin often shows up as the classical age-related changes we all think of: deep wrinkles, sallow discoloration, and irregular pigmentation.

Photo-aging occurs because UV light from the sun is divided into UV-A and UV-B. UV-A damages the deeper layers of the skin while UV-B causes sunburns on the outer layers. Collagen in the deeper layers of the skin can also be damaged by enzymes called “metallo-proteinases” which are turned on by UV sunlight. Oxidation plays an important role in the way that UV light damages the skin, doubling your need for the crucial antioxidants that reverse this process.

Topical agents typically focus on antioxidant support to reduce the damage from sun and elements. This can help mitigate extrinsic aging. But having an antioxidant rich diet and supplementing properly takes this all a very big step further. Taking these additional steps can help both intrinsic and extrinsic” aging, giving you more bang for your buck.

So to get the most out of your anti-aging program, here is what I recommend:

Consume large amounts of richly-colored vegetables as close as possible to their original uncooked raw form. Richly-colored plants contain phytochemicals of which many are potent anti-oxidants.

Use sunscreen. This helps protect your skin from the effects of UV light.

Don’t smoke.

Consume moderate amounts of alcohol.

Supplement

When it comes to supplementation a great way to kick start your program is to try and IV infusion designed enhance collagen synthesis and protect your skin, like the Skin and Collagen IV Treatment at our clinic in Newport Beach, CA. It also provides your body a fast replacement of the nutrients your skin needs. This helps stop and reverse the aging process. Once your base levels of these nutrients are remediated, you can maintain them with oral Liposomal Vitamin C, Liposomal Glutathione and other supplements discussed in this post (see below).

There are a few key nutrients that play a crucial role in skin health. You should consider the following as you are creating a supplement plan for your skin and your overall health.

8 Key Skin Nutrients:

1. Vitamin A (retinol—the active form of Vitamin A)…

Vitamin A is required for maintaining many essential physiological processes in the body including normal growth and development, normal vision, a healthy immune system, normal reproduction, and healthy skin and barrier functions. In excess of 500 genes are thought to be regulated by retinol.

Vitamin A is beneficial in the treatment of acne, “liver spots”, wrinkles and rough skin. One study showed that 0.4% retinol applied topically had promising anti-aging benefits (2)

UV light depletes the skin of Vitamin A. So it’s clear why this vitamin is part of anti-aging and skin improvement formulas.

It’s always a good idea to test your levels of vitamins, minerals and antioxidants before you begin treatment. If you are low in Vitamin A, a good way to get your retinol levels up quickly is to take 500,000 units per day orally for 3 days, 250,000 units for the next 3 days, 125,000 units for the next 3 days and then maintain on 60,000 units. You also should continue to test your Vitamin A levels periodically as this is a fat soluble vitamin and can accumulate to toxic levels. AVOID VITAMIN A THERAPY COMPLETELY IF YOU ARE PREGNANT

2. Niacinamide (B3 also called nicotinamide):

Niacinamide helps with moisture retention in the skin. Topically, applied niacinamide (also known as nicotinamide) 2-4% is also an effective skin whitener. Nicotinamide, an amide form of vitamin B3, boosts cellular energy and regulates poly-ADP-ribose-polymerase 1, an enzyme with important roles in DNA repair and the expression of inflammatory cytokines (3)

Nicotinamide shows promise for the treatment of a wide range of dermatological conditions, including autoimmune blistering disorders, acne, rosacea, aging skin and atopic dermatitis.

In particular, recent studies have also shown it to be a potential agent for reducing actinic keratoses and preventing skin cancers (4). Oral nicotinamide was also found to be safe and effective in reducing the rates of new non-melanoma skin cancers and actinic keratoses in high-risk patients.

3. Dexpanthenol (B5)

Like Niacinamide, Vitamin B5 is also important in maintaining tissue hydration. It reduces cholesterol levels and inflammation as well through the production of Acetyl CoA. B5 also regulates keratinocyte proliferation.

In a study, topical B5 5% ointment was as effective as 1% hydrocortisone treatment in mild to moderate atopic dermatitis (eczema) (5). Also, giving B5 orally may help decrease facial acne as shown in a study of 48 patients (6).

There is no known upper limit known for B5 supplementation, and there are lots of protocols online of high dose B5 to treat acne. For example, 5-10 grams per day has been shown to decrease acne as per Dr. Leung’s protocol, but this is not a published study by any means. Some are reporting it as effective as the commercial drug Accutane but without the major side effects.

However, one possible side effect of high dose B5 to be aware of is that stool will turn green (from bile dumping), and this may be accompanied by abdominal pain and bloating. An alternative protocol to the very high dose B5 is to use a smaller dose of B5 and combine it with L-carnitine. This may be particularly effective in treating oily skin problems as B5 decreases the accumulation of fat/oil in the skin and L-carnitine helps shuttle the fatty acids into the mitochondria to be used as energy.

In IV form B5 can be used in high doses of 500-1000 mg per IV once or twice per week. B5 is already one of the main ingredients in many of the treatments in our IV Vitamin Therapy Clinic and we often customize and individualize each IV infusion to the particular needs of our patient. WE can add a high dose of Vitamin B5 for example to almost any of the existing treatments if in fact we feel it is necessary.

4. Vitamin C

Vitamin C, also known as Ascorbic Acid, is a very important antioxidant known to reduce the photo-aging because it protects against UV light damage. It also plays an integral role in collagen production.

Topical Vitamin C:

• Reduces wrinkling in as little as 2 weeks

• Decreases the activity of melanocytes, which means it is an effective treatment in de-pigmentation of the skin,

• Decreases skin roughness

• Is effective only if the topical cream has a pH below 3.5 and only the L-ascorbic acid form is effective so make sure to check the ingredients.

• Is available in concentrations of 3-10%. However, many get the maximum benefit from 20% concentrations.

• Rarely can cause rash and can be applied every 8 hours. It’s half-life is 4 days.

• Is safe to use with other agents like glycolic acid, sunscreen etc.

Increased intake of oral Vitamin C is associated with decreased skin dryness. When taking oral Ascorbic Acid I recommend using Liposomal Vitamin C which is a vitamin encapsulation technology allowing up to 90% absorption.

IV infusions with Vitamin C are very easy to tolerate and have the added effect of increasing overall energy and vitality.

5. Minerals

Minerals are important in skin formation and protection. Mineral oxides (such as Zinc Oxide) absorb UV light and protect the deeper levels of skin from damage. Of the essential minerals, selenium and zinc have been studied most extensively when it comes to their impact on skin. Both appear to be important in protecting the skin from photo-aging and free radical damage (8).

Zinc stabilizes cell membranes and is important in cell division. This can help in wound healing. Zinc oxide and Zinc titanium are commonly found in sunscreens.

Selenium plays an important part in antioxidant proteins like glutathione peroxidase (PHGPx) and Thioredoxin Reductase (TDR) which protect skin cells from free radicals. Selenium is also key in recycling the master anti-oxidant glutathione. Selenium is present in many dandruff shampoo formulations as well.

6. Amino Acids

The amino acids L-lysine and L-proline are an integral part of collagen molecule and collagen forms the base layer of skin. However other branched chain amino acids (BCAA’s) and L-Glutamine may also play a role in collagen formation. UV Light exposure decreases the formation of new collagen and needs to be counteracted. Supplementing with key amino acids may help reverse this process. In one animal study (9) BCAA’s, L-Glutamine and proline administered orally were able to increase collagen synthesis which was initially decreased by using UV light exposure.

7. Glutathione

Glutathione is a major antioxidant in the body and plays a critical role in Phase II detoxification pathways in the body. This means it inactivates toxic molecules like heavy metals and makes them more water soluble, so that the kidneys can then flush them out.

Glutathione also has a reputation for skin whitening (10). Importantly, it inhibits melanin formation (melanin is the pigment in skin) by suppressing the activity of an enzyme called tyrosinase.

A 2012 double-blind study of 60 participants taking 500 mg reduced glutathione for 4 weeks saw reduced melanin production at 6 different skin sites (11). In another double-blind placebo controlled study in 2014, 30 participants used 2% oxidized (inactive) topical glutathione for 10 weeks and achieved a significantly lower melanin index (whitening) (12) To be fair however, two 2016 studies dispute the effect glutathione has on inhibiting melanin.(13,14)

While there are no current studies on the effect of IV Glutathione treatments for skin whitening, we do know that glutathione has a protective effect on skin through its antioxidant effect and it is considered safe even in very large doses—much higher than the typical 600-1000 mg IV doses used in IV clinics throughout the world including our clinic, IV for Life, in Newport Beach, CA.

Many patients report an evening out of their complexion, better skin tone and moisture after IV Glutathione treatments.

When taking glutathione orally I recommend only using Liposomal Glutathione, as plain glutathione has very poor absorption due to destruction by bile and stomach acid.

8. CoQ10

Coenzyme Q 10 (CoQ10) may have positive effects on photo-aging, wrinkles, skin spots, dryness and tumors. This is because it is a powerful antioxidant which neutralizes the free radicals induced by UV light which are thought to be a major factor that initiate the up-regulation of matrix metalloproteinases (MMPs). MMP’s are enzymes present in fluctuating levels in keratinocytes and fibroblasts in the deeper levels of skin.

MMP’s damage the collagen structure of skin and degrade it causing a wrinkled, aged look. A 2008 study of topically applied 1% CoQ10 cream found that the subjects had a significant reduction of wrinkles, and it is thought that this was caused by CoQ10’s antioxidant action. In addition CoQ10 inhibits MMP production, protecting dermal fiber components from degradation, leading to rejuvenation of wrinkled skin (15).

CoQ10 is easily absorbed by mouth and can be very helpful in energy production. It is depleted by “statins” which are popular prescription medications used to lower cholesterol and should definitely be used in conjunction with these medications. CoQ10 is also available as a intramuscular (IM) shot or as an IV infusion at our clinic IV for Life.

By eating well, and taking the right supplements (along with the other lifestyle tips noted above), you can get that glowing, beautiful skin you have always wanted, reverse the signs of aging and enhance your overall health at the same time.

References

 Skin-whitening and skin-condition-improving effects of topical oxidized glutathione: a double-blind and placebo-controlled clinical trial in healthy women. Clinical, cosmetic and investigational dermatology. 2014.

2) Molecular basis of retinol anti-aging properties in naturally aged human skin in vivo.

Int J. Cosmetic Sci. 2016

3 Nicotinamide and The Skin Austrealas. J Dermatol. 2014.

4 A Phase 3 Randomized Trial of Nicotinamide for Skin-Cancer Chemoprevention. N Engl J Med. 2015.

5 Comparative trial of 5% dexpanthenol in water-in-oil formulation with 1% hydrocortisone ointment in the treatment of childhood atopic dermatitis: a pilot study. J Drugs Dermatol. 2012.

6 A randomized, double-blind, placebo-controlled study of a novel pantothenic Acid-based dietary supplement in subjects with mild to moderate facial acne. Dermatol Ther 2014.

7 Vitamin C in dermatology. Indian Dermatol Online J. 2013

8 Linus Pauling Institute – Micronutrient Information Center http://lpi.oregonstate.edu/mic/micronutrients-health/skin-health/nutrient-index/minerals

9 Importance of amino acid composition to improve skin collagen protein synthesis rates in UV-irradiated mice Amino Acids. 2012.

10 Glutathione as a skin whitening agent: Facts, myths, evidence and controversies Indian J. Dermatol 2016

11 Glutathione as an oral whitening agent: a randomized, double-blind, placebo-controlled study. J Dermatolog Treat 2012.

12 Skin-whitening and skin-condition-improving effects of topical oxidized glutathione: a double-blind and placebo-controlled clinical trial in healthy women

Clin Cosmet Investig Dermatol. 2014.

13 Glutathione as a depigmenting agent: an overview. Int. J Cosmet. Sci 2005.

14 The Glutathione Derivative, GSH Monoethyl Ester, May Effectively Whiten Skin but GSH Does Not. Int J Mol Sci. 2016.

15 Mechanisms of inhibitory effects of CoQ10 on UVB-induced wrinkle formation in vitro and in vivo. Biofactors 2008.

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Thuốc Acemuc kids tác dụng, liều dùng, giá bao nhiêu? | Tracuuthuoctay

TraCuuThuocTay.com chia sẻ: Thuốc Acemuc kids điều trị bệnh gì?. Acemuc kids công dụng, tác dụng phụ, liều lượng.

BÌNH LUẬN cuối bài để biết: Thuốc Acemuc kids giá bao nhiêu? mua ở đâu? Tp HCM, Hà Nội, Cần Thơ, Bình Dương, Đồng Nai, Đà Nẵng. Vui lòng tham khảo các chi tiết dưới đây.

Acemuc kids

Tác giả: Ths.Dược sĩ Phạm Liên Tham vấn y khoa nhóm biên tập. ngày cập nhật: 9/8/2019

Nhóm thuốc: Thuốc tác dụng trên đường hô hấp

Dạng bào chế:Thuốc cốm

Thành phần:

Mỗi 0,5g chứa: Acetylcystein 100mg

SĐK:VD-33019-19

Nhà sản xuất: Công ty Cổ phần Dược phẩm Sanofi Việt Nam – VIỆT NAM Nhà đăng ký: Công ty Cổ phần Dược phẩm Sanofi Việt Nam Nhà phân phối:

Chỉ định:

Hỗ trợ điều trị trong các trường hợp viêm đường hô hấp kèm dịch đờm nhày.

Giải độc trong quá liều paracetamol

TÁC DỤNG

N-Acetyl cystein có tác dụng cắt đứt các cầu nối S-S của dich nhày đờm ở đường hô hấp, cùng với phản xạ ho giúp đẩy chất đờm ra ngoài.

N-Acetyl cystein còn có tác dụng là thuốc giải độc khi quá liều paracetamol. Sau khi vào cơ thể N-Acetyl cystein chuyển hóa thành acetylcystein kích thích gan tổng hợp glutathion do đó duy trì hoặc khôi phục nồng độ glutathion của gan là chất cần thiết để làm bất hoạt chất chuyển hóa trung gian của paracetmol gây độc cho gan. Vì vậy có thể bảo vệ gan nếu được điều trị sớm.

Liều lượng – Cách dùng

Trẻ em dưới 2 tuổi: uống 200mg/ ngày chia 2 lần

Trẻ 2-6 tuổi: uống 200mg/2 lần/ ngày

Hoặc dùng theo chỉ dẫn bác sĩ

QUÁ LIỀU VÀ XỬ TRÍ

Triệu chứng: quá liều N-Acetyl cystein có triệu chứng giống như sốc phản vệ, nhưng nặng hơn đặc biệt là tụt huyết áp, suy hô hấp.

Xử trí: điều trị triệu chứng

Chống chỉ định:

Mẫn cảm với hoạt chất N-Acetyl cystein và bất kì thành phần nào của thuốc.

Những bệnh hen có nguy cơ xuất hiện phản ứng co thắt phế quản với tất cả các dạng thuốc chứa acetylcystein.

Tương tác thuốc:

N-Acetyl cystein là một chất khử nên không dùng kèm với các chất có tính oxy hóa như các kim loại có tính oxy hóa mạnh ( sắt, nhôm)

Không dùng đồng thời với các thuốc ho khác hoặc các thuốc làm giảm bài tiết phế quản trong thời gian điều trị với N-Acetyl cystein

Tương kị với các dung dịch chứa penicilin, oxacillin, ampjotericin B, tetracyclin.

Tác dụng phụ:

N-Acetyl cystein là thuốc có giới hạn an toàn rộng, một số tác dụng phụ như sau

Buồn nôn, nôn.

Buồn ngủ, nhức đầu, ù tai.

Hiếm gặp: co thắt khí phế quản , sốt, rét run. Phản ứng quá mẫn.

Chú ý đề phòng:

Giám sát những bệnh nhân có tiền sử hen khi dùng thuốc, nếu có hiện tượng co thắt khí phế quản phải ngừng thuốc ngay và điều trị triệu chứng với thuốc giãn phế quản (salbutamol)

Với những bệnh nhân không có khả năng khạc nhổ đờm, khi dùng với thuốc đờm sẽ loãng vì vậy cần hút đờm giúp bệnh nhân

Thông tin thành phần Acetylcystein

Dược lực:

Acetylcystein là một chất điều hòa chất nhầy theo kiểu làm tan đàm. Thuốc tác động trên giai đoạn gel của niêm dịch bằng cách cắt đứt cầu nối disulfur của các glycoprotein.

Dược động học :

Sau khi hít qua miệng hoặc nhỏ thuốc vào khí quản, phần lớn thuốc tham gia vào phản ứng sulfhydryl – disulfid, số còn lại được biểu mô phổi hấp thu. Sau khi uống, acetylcystein được hấp thu nhanh ở đường tiêu hóa và bị gan khử acetyl thành cystein và sau đó được chuyển hóa. Ðạt nồng độ đỉnh huyết tương trong khoảng 0,5 đến 1 giờ sau khi uống liều 200 đến 600 mg. Khả dụng sinh học khi uống thấp và có thể do chuyển hóa trong thành ruột và chuyển hóa bước đầu trong gan. Ðộ thanh thải thận có thể chiếm 30% độ thanh thải toàn thân. Sau khi tiêm tĩnh mạch, nửa đời cuối trung bình là 1,95 và 5,58 giờ tương ứng với acetylcystein khử và acetylcystein toàn phần; sau khi uống, nửa đời cuối của acetylcystein toàn phần là 6,25 giờ.

Tác dụng :

Acetylcystein (N – acetylcystein) là dẫn chất N – acetyl của L – cystein, một amino – acid tự nhiên. Acetylcystein được dùng làm thuốc tiêu chất nhầy và thuốc giải độc khi quá liều paracetamol. Thuốc làm giảm độ quánh của đờm ở phổi có mủ hoặc không bằng cách tách đôi cầu nối disulfua trong mucoprotein và tạo thuận lợi để tống đờm ra ngoài bằng ho, dẫn lưu tư thế hoặc bằng phương pháp cơ học. Acetylcystein cũng được dùng tại chỗ để điều trị không có nước mắt. Acetylcystein dùng để bảo vệ chống gây độc cho gan do quá liều paracetamol, bằng cách duy trì hoặc khôi phục nồng độ glutathion của gan là chất cần thiết để làm bất hoạt chất chuyển hóa trung gian của paracetamol gây độc cho gan. Trong quá liều paracetamol, một lượng lớn chất chuyển hóa này được tạo ra vì đường chuyển hóa chính (liên hợp glucuronid và sulfat) trở thành bão hòa. Acetylcystein chuyển hóa thành cystein kích thích gan tổng hợp glutathion và do đó, acetylcystein có thể bảo vệ được gan nếu bắt đầu điều trị trong vòng 12 giờ sau quá liều paracetamol. Bắt đầu điều trị càng sớm càng tốt.

Chỉ định :

Ðược dùng làm thuốc tiêu chất nhầy trong bệnh nhầy nhớt (mucoviscidosis) (xơ nang tuyến tụy), bệnh lý hô hấp có đờm nhầy quánh như trong viêm phế quản cấp và mạn, và làm sạch thường quy trong mở khí quản. 

Ðược dùng làm thuốc giải độc trong quá liều paracetamol. Ðược dùng tại chỗ trong điều trị hội chứng khô mắt (viêm kết giác mạc khô, hội chứng Sjogren) kết hợp với tiết bất thường chất nhầy.

Liều lượng – cách dùng:

Cách dùng: Nếu dùng làm thuốc tiêu chất nhầy, có thể phun mù, cho trực tiếp hoặc nhỏ vào khí quản dung dịch acetylcystein 10 – 20%. Thuốc tác dụng tốt nhất ở pH từ 7 đến 9, và pH của các chế phẩm bán trên thị trường có thể đã được điều chỉnh bằng natri hydroxyd. Nếu dùng làm thuốc giải độc trong quá liều paracetamol, có thể cho uống dung dịch acetylcystein 5%. Cũng có thể dùng đường tiêm nhỏ giọt tĩnh mạch để điều trị quá liều paracetamol nhưng nên chọn cách uống. Thuốc nhỏ mắt acetylcystein 5% dùng tại chỗ để làm giảm nhẹ các triệu chứng do thiếu màng mỏng nước mắt. Liều lượng: Làm thuốc tiêu chất nhầy, acetylcystein có thể được dùng: Hoặc phun mù 3 – 5 ml dung dịch 20% hoặc 6 – 10 ml dung dịch 10% qua một mặt nạ hoặc đầu vòi phun, từ 3 đến 4 lần mỗi ngày. Nếu cần, có thể phun mù 1 đến 10 ml dung dịch 20% hoặc 2 đến 20 ml dung dịch 10%, cách 2 đến 6 giờ 1 lần. Hoặc nhỏ trực tiếp vào khí quản từ 1 đến 2 ml dung dịch 10 đến 20% mỗi giờ 1 lần. Có thể phải hút đờm loãng bằng máy hút. Hoặc uống với liều 200 mg, ba lần mỗi ngày, dưới dạng hạt hòa tan trong nước. Trẻ em dưới 2 tuổi uống 200 mg/ngày chia 2 lần và trẻ em từ 2 đến 6 tuổi uống 200 mg, hai lần mỗi ngày. Ðiều trị khô mắt có tiết chất nhầy bất thường: Thường dùng acetylcystein tại chỗ, dưới dạng dung dịch 5% cùng với hypromellose, nhỏ 1 đến 2 giọt, 3 đến 4 lần mỗi ngày. Dùng làm thuốc giải độc quá liều paracetamol bằng cách tiêm truyền tĩnh mạch hoặc uống: Tiêm truyền tĩnh mạch: Liều đầu tiên 150 mg /kg thể trọng, dưới dạng dung dịch 20% trong 200 ml glucose 5%, tiêm tĩnh mạch trong 15 phút, tiếp theo, truyền nhỏ giọt tĩnh mạch 50 mg/kg trong 500 ml glucose 5%, trong 4 giờ tiếp theo và sau đó 100 mg/kg trong 1 lít glucose 5% truyền trong 16 giờ tiếp theo. Ðối với trẻ em thể tích dịch truyền tĩnh mạch phải thay đổi. Hoặc uống: Liều đầu tiên 140 mg/kg, dùng dung dịch 5%; tiếp theo cách 4 giờ uống 1 lần, liều 70 mg/kg thể trọng và uống tổng cộng thêm 17 lần. Acetylcystein được thông báo là rất hiệu quả khi dùng trong vòng 8 giờ sau khi bị quá liều paracetamol, hiệu quả bảo vệ giảm đi sau thời gian đó. Nếu bắt đầu điều trị chậm hơn 15 giờ thì không hiệu quả, nhưng các công trình nghiên cứu gần đây cho rằng vẫn còn có ích.

Chống chỉ định :

Tiền sử hen (nguy cơ phản ứng co thắt phế quản với tất cả các dạng thuốc chứa acetylcystein). Quá mẫn với acetylcystein.

Tác dụng phụ

Acetylcystein có giới hạn an toàn rộng. Tuy hiếm gặp co thắt phế quản rõ ràng trong lâm sàng do acetylcys-tein, nhưng vẫn có thể xảy ra với tất cả các dạng thuốc chứa acetylcystein. – Thường gặp: Buồn nôn, nôn. – Ít gặp: Buồn ngủ, nhức đầu, ù tai. Viêm miệng, chảy nước mũi nhiều. Phát ban, mày đay. – Hiếm gặp: Co thắt phế quản kèm phản ứng dạng phản vệ toàn thân. Sốt, rét run. Hướng dẫn cách xử trí tác dụng không mong muốn: Dùng dung dịch acetylcystein pha loãng có thể giảm khả năng gây nôn nhiều do thuốc. Phải điều trị ngay phản ứng phản vệ bằng tiêm dưới da adrenalin (0,3 – 0,5 ml dung dịch 1/1000 ) thở oxy 100%, đặt nội khí quản nếu cần, truyền dịch tĩnh mạch để tăng thể tích huyết tương, hít thuốc chủ vận beta – adrenergic nếu co thắt phế quản, tiêm tĩnh mạch 500 mg hydrocortison hoặc 125 mg methylprednisolon. Có thể ức chế phản ứng quá mẫn với acetylcystein bao gồm phát hồng ban toàn thân, ngứa, buồn nôn, nôn, chóng mặt, bằng dùng kháng histamin trước. Có ý kiến cho rằng quá mẫn là do cơ chế giả dị ứng trên cơ sở giải phóng histamin hơn là do nguyên nhân miễn dịch. Vì phản ứng quá mẫn đã xảy ra tới 3% số người tiêm tĩnh mạch acetylcystein để điều trị quá liều paracetamol, nên các thầy thuốc cần chú ý dùng kháng histamin để phòng phản ứng đó.

Lưu ý: Dùng thuốc theo chỉ định của Bác sĩ

Nguồn tham khảo drugs.com, medicines.org.uk, webmd.com và TraCuuThuocTay.com tổng hợp.

Cần tư vấn thêm về Thuốc Acemuc kids tác dụng, liều dùng, giá bao nhiêu? bình luận cuối bài viết.

Tuyên bố miễn trừ trách nhiệm y tế

Nội dung của TraCuuThuocTay.com chỉ nhằm mục đích cung cấp thông tin về Thuốc Acemuc kids tác dụng, liều dùng, giá bao nhiêu? và không nhằm mục đích thay thế cho tư vấn, chẩn đoán hoặc điều trị y tế chuyên nghiệp.

Chúng tôi miễn trừ trách nhiệm y tế nếu bệnh nhân tự ý sử dụng thuốc mà không tuân theo chỉ định của bác sĩ.

Vui lòng liên hệ với bác sĩ hoặc phòng khám, bệnh viện gần nhất để được tư vấn.

Đánh giá 5* post

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