#Electron transport chain

[tenth-sentence]

Cyanide inhibits cytochrome c oxidase in the mitochondria, which blocks the electron transport chain.

"Plant Physiology and Development" int'l 6e - Taiz, L., Zeiger, E., Møller, I.M., Murphy, A.

[whats-in-a-sentence]

In summary, plant respiratory rates are allosterically controlled from the "bottom up" by the cellular level of ADP (Figure 12.13).

"Plant Physiology and Development" int'l 6e - Taiz, L., Zeiger, E., Møller, I.M., Murphy, A.

[illarian-rambling]

Study sesh so bad I had to go on a walk to bask in the glory of nature

[photmath]

ended up getting a 97.5 on that exam, god I love being a woman in stem

[blueoaknx]

The Story of Mitochondria: Evolution, Function, and Molecular Machinery

Mitochondria are double-membraned organelles that play an essential role in cellular bioenergetics and various metabolic pathways. Known primarily as the “powerhouses of the cell,” mitochondria generate most of the cell’s adenosine triphosphate (ATP) through oxidative phosphorylation (OXPHOS). Beyond energy production, these organelles regulate several crucial functions, including apoptosis, calcium signaling, and reactive oxygen species (ROS) management. This article delves into the technical aspects of mitochondrial evolution, structure, functions, and their involvement in disease, illuminating why these unique organelles are pivotal to cellular health.

Evolutionary Origins: The Endosymbiotic Theory and Genome Reduction

Mitochondria originated from an ancient symbiotic event approximately 1.5–2 billion years ago, when an ancestral eukaryotic cell engulfed a free-living, aerobic bacterium. This theory, known as the endosymbiotic theory, was proposed by biologist Lynn Margulis in the 1960s and has been widely substantiated by evidence from molecular biology and genetics. The engulfed bacterium eventually became an organelle within the host cell, providing a selective advantage by supplying ATP through aerobic respiration.

Over evolutionary time, mitochondrial DNA (mtDNA) underwent significant gene reduction, as many genes were either lost or transferred to the nuclear genome. The modern human mitochondrial genome is compact, with only 37 genes remaining, encoding 13 proteins essential for oxidative phosphorylation, 22 transfer RNAs (tRNAs), and 2 ribosomal RNAs (rRNAs). Most of the proteins required for mitochondrial function are now encoded by nuclear DNA and imported into the mitochondria via translocases and specialized import machinery. This gene reduction reflects a co-evolution of mitochondria with the eukaryotic host, solidifying their role as a semi-autonomous organelle within eukaryotic cells.

Structure and Compartments of Mitochondria

Mitochondria have a highly specialized structure, featuring a double membrane that divides them into distinct compartments: the outer membrane, intermembrane space, inner membrane, and matrix. This compartmentalization enables spatial separation of various metabolic processes and facilitates the generation of a proton gradient necessary for ATP synthesis.

Outer Membrane: The outer mitochondrial membrane contains porins—integral membrane proteins that allow the free diffusion of molecules up to 5 kDa. This membrane also contains enzymes involved in lipid synthesis and oxidation. The voltage-dependent anion channel (VDAC) is a key protein of the outer membrane, mediating metabolite exchange and regulating ion permeability.

Intermembrane Space: The intermembrane space lies between the outer and inner membranes and contains enzymes involved in processes such as nucleotide phosphorylation. It also plays a critical role in the apoptosis pathway, as cytochrome c and other pro-apoptotic factors are released into this space before initiating the apoptotic cascade.

Inner Membrane: The inner membrane is rich in proteins and contains the electron transport chain (ETC) complexes, which carry out oxidative phosphorylation. This membrane is impermeable to most ions and molecules, ensuring that the proton gradient established by the ETC is maintained. The inner membrane’s distinctive folds, known as cristae, increase the surface area available for oxidative phosphorylation and house the complexes I-IV, ATP synthase, and various other transport proteins.

Matrix: The mitochondrial matrix is the innermost compartment and contains enzymes for the tricarboxylic acid (TCA) cycle, mtDNA, ribosomes, and tRNAs. The matrix environment is essential for mitochondrial gene expression and also serves as a site for other metabolic reactions, such as fatty acid oxidation and amino acid synthesis.

Oxidative Phosphorylation and ATP Production

The primary function of mitochondria is to produce ATP through the process of oxidative phosphorylation, which occurs in the inner membrane and involves the electron transport chain (ETC) and ATP synthase.

Electron Transport Chain (ETC): The ETC comprises four protein complexes (Complexes I-IV) that facilitate the transfer of electrons from electron carriers NADH and FADH₂ to molecular oxygen (O₂). Complex I (NADH dehydrogenase) and Complex II (succinate dehydrogenase) initiate electron transfer, followed by Complex III (cytochrome bc₁ complex) and Complex IV (cytochrome c oxidase). As electrons pass through these complexes, protons (H⁺) are pumped from the matrix to the intermembrane space, creating an electrochemical gradient across the inner membrane.

ATP Synthase: The proton gradient generated by the ETC drives the synthesis of ATP via ATP synthase (Complex V), a molecular motor that converts ADP and inorganic phosphate (Pi) into ATP. As protons flow back into the matrix through ATP synthase, the energy released is used to phosphorylate ADP. This process, chemiosmosis, is central to ATP production and is the primary source of energy in eukaryotic cells.

Mitochondrial DNA and Genetic Regulation

Mitochondrial DNA (mtDNA) encodes a small but essential portion of the proteins required for mitochondrial function. Mitochondrial genes are transcribed within the matrix by mitochondrial RNA polymerase, and translation occurs on specialized mitochondrial ribosomes that resemble bacterial ribosomes. Despite their independence in certain functions, mitochondria rely heavily on nuclear-encoded proteins, which are imported into the organelle through translocase complexes (TOM and TIM) on the outer and inner membranes, respectively.

Notably, mtDNA has a high mutation rate due to limited DNA repair mechanisms and exposure to reactive oxygen species (ROS) generated during oxidative phosphorylation. Mutations in mtDNA can lead to defects in ETC complexes, impairing ATP production and resulting in a range of mitochondrial diseases.

Regulatory Roles Beyond Energy Production

In addition to ATP synthesis, mitochondria regulate several essential cellular processes, including:

Apoptosis: Mitochondria play a central role in programmed cell death (apoptosis) through the release of cytochrome c and other pro-apoptotic factors from the intermembrane space. Once in the cytoplasm, cytochrome c binds to Apaf-1, leading to caspase activation and cell death.

Calcium Signaling: Mitochondria act as calcium reservoirs, modulating intracellular calcium levels by sequestering and releasing Ca²⁺. The mitochondrial calcium uniporter (MCU) imports Ca²⁺ into the matrix, influencing metabolic activity by activating TCA cycle enzymes.

Reactive Oxygen Species (ROS) Production: Mitochondria are the primary source of ROS in cells, especially superoxide (O₂•⁻), which is produced during electron transfer in the ETC. Mitochondria contain antioxidant enzymes like superoxide dismutase (SOD) and glutathione peroxidase to neutralize ROS. However, excessive ROS can lead to oxidative stress, damaging cellular structures, mtDNA, and contributing to aging and degenerative diseases.

Mitochondrial Dysfunction and Disease

Mitochondrial dysfunction can result from mtDNA mutations, nuclear DNA mutations, or environmental factors that impair the ETC and ATP production. This dysfunction is implicated in numerous disorders:

Mitochondrial Myopathies: These disorders affect skeletal muscle, leading to muscle weakness and fatigue. Mutations in mtDNA or nuclear DNA affecting ETC proteins often underlie these diseases.

Neurodegenerative Diseases: Impaired mitochondrial function is associated with neurodegenerative conditions like Parkinson’s, Alzheimer’s, and Huntington’s diseases. Mitochondrial dysfunction in neurons leads to reduced ATP production, increased oxidative stress, and apoptosis, all contributing to neurodegeneration.

Cardiovascular Diseases and Aging: Age-related decline in mitochondrial function and mtDNA mutations contribute to reduced ATP production and increased ROS. This decline is associated with sarcopenia, cognitive aging, and increased susceptibility to cardiovascular diseases.

Advances in Mitochondrial Research

Research on mitochondrial therapeutics is advancing, focusing on treatments that can enhance mitochondrial function or compensate for defects. Approaches such as mitochondrial replacement therapy (MRT), antioxidant therapy, and targeted gene editing are under investigation. Lifestyle factors, including diet and exercise, have also been shown to positively influence mitochondrial function, providing non-invasive strategies to support mitochondrial health.

Conclusion

The technical story of mitochondria encompasses their unique evolutionary origin, complex structure, and multifaceted roles in cellular homeostasis. Far beyond simple energy producers, mitochondria are integral to cellular regulation, signal transduction, and apoptosis. As research progresses, understanding the intricate molecular machinery and regulation of mitochondria holds promise for developing therapies for mitochondrial diseases and conditions linked to aging.

[autumnoakes]

glycolysis,,,,,, *shakes fist*

[the-good-arsonist]

Adenosine triphosphate

In my science era. cells and stuff

[pharmaguidelines]

Electron transport chain (ETC) Pathway

Electron Transport Chain (ETC): A Powerhouse for Cellular Energy In the bustling world of cells, energy is the lifeblood that drives every process, from building proteins to transporting nutrients. And one of the most crucial players in this energy-generating game is the Electron Transport Chain (ETC). Imagine the ETC as a miniature power plant within the cell’s powerhouse, the mitochondria.…

[lesbianssasuke]

just spent the past 7 hrs for a total of 10 hrs working on coding for my stats midterm i dont wanna be a cs girly this is terrible

[stuckinapril]

glycolysis gluconeogenesis glycogenesis krebs cycle electron transport chain fermentation pentose phosphate pathway fatty acid synthesis fatty acid oxidation molecular cloning native gels sds-page gel electrophoresis tissue specific metabolism cholesterol metabolism ketone bodies recombinant dna and biotechnology zeroth law of thermodynamics hydrostatics fluid dynamics fluids in physiology nuclear binding energy and mass defect nuclear reactions consciousness-altering drugs drug addiction and the reward pathway in the brain the role of emotion in retrieving memories retrieval cues neural plasticity james-lange theory cannon-bard theory schachter-singer theory biological bases of behavior genetically based behavioral variation in natural populations psychoanalytic perspective dissociative disorders trauma and stressor related disorders drive reduction theory incentive theory bystander effect social loafing habituation and dishabituation operant conditioning fixed-ratio reinforcement prejudice and bias individual vs institutional discrimination microsociology vs macrosociology theories of demographic change.......................

[tenth-sentence]

The individual electron transport proteins are organized into four transmembrane multiprotein complexes (identified by roman numerals I through IV), all of which are localized in the inner mitochondrial membrane.

"Plant Physiology and Development" int'l 6e - Taiz, L., Zeiger, E., Møller, I.M., Murphy, A.

[whats-in-a-sentence]

The up-regulation of alternative oxidase is an example of retrograde regulation, in which nuclear gene expression responds to changes in organellar status (Figure 12.11). (...) Taken together, these NADH hydrogenases and the NADPH dehydrogenases are likely to make plant respiration more flexible and allow control of specific redox homeostasis of NADH and NADPH in mitochondria and cytosol (see Figure 12.11). (...) Of special importance is the synthesis of ascorbic acid, a central redox and stress defense molecule in plants, by the electron transport chain (see Figure 12.11).

"Plant Physiology and Development" int'l 6e - Taiz, L., Zeiger, E., Møller, I.M., Murphy, A.

[zolanort]

A hypothesis regarding the discolored monster blood in LU

We will be working with the assumption that blood in Hyrule has the same general functions that it does on earth. Our heroes are shown to bleed red and seem to expect blood in general to be not-dark at the very least. Based on earth, red/hemoglobin is the most popular option, though green/chlorocruorin and blue/hemocyanin do seem to be on the table based on my N64 save files.

Bad guys like to have their bases in cool places like volcanos. If Dink is set up near a volcano (+10 points for aesthetic) he and his minions could be suffering from Sulfhemoglobinemia. Sulphur can bind to hemoglobin, causing the affected blood to appear darker in color. If this were the case, however, we would expect the dark blooded monsters to be weaker because their blood would be less efficient at carrying oxygen, and therefore this option is unlikely as the black blooded monsters are shown to be stronger than regular monsters. Also the blood wouldn’t be black exactly, but a darker blue-green, so this probably isn’t the culprit.

Having low oxygen levels in general would cause blood to appear darker (darker red, not blue), but just like above, this would leave the monsters weaker rather than stronger, and therefore this option is highly unlikely.

The dark blooded monsters are referred to as being “infected” and Wind even asks if they’re sick.

Our sailor is a smart pirate lad; infections can and do cause blood discolorations, but this is usually due to the presence of something extra in the mix (which is basically always bad/not going to give you a power boost) and/or the usual problem where the red blood cells are rendered less efficient at their oxygen carrying duties, causing a darker red color. Therefore, a straight forward infection involving a biological agent (bacteria etc.) is not likely.

Blood will oxidize when it is old, which could make it appear dark/black in coloration. This doesn’t really support being extra strong or even alive, but this is the option I think is most likely. Why?

Because magic. This isn’t news, we all knew it was magic already. The Bad Guys are being fueled by an evil dark magical infection of some kind. But why black blood and a power boost specifically?

Assuming that magic is a form of energy, I propose that their cellular respiration may have been magically converted to use the evil dark magic instead of ATP. Why? With a (seemingly?) infinite supply of anger and spite fueled dark energy rather than a limited amount of ATP, and also assuming that dark energy wouldn’t impact the electron transport chain like ATP and the associated energy exchange byproducts would, the muscles of an infected monster would never get tired. This addresses our key issue of explaining the power boost symptom.

While any of the other coloration causes above could work along with this idea, due to the citric acid cycle being eliminated from the picture (and the need for breathing/oxygen along with it), the red blood cells are probably just chilling in the evil darkness infused veins of the baddies, aging and then not really doing anything else until the blood is lost via fighting the heroes. This would explain both the dark coloration and why this symptom is directly tied to the evil dark magic and the associated power boost.

Anyway they probably just have discolored blood for evil dark magic aesthetic purposes, which is also cool, but it was fun to try to create an explanation.

[gray-matter-in-a-teacup]

Cyanide Poison

Let's start by understanding exactly how cyanide kills you. In simple terms, cyanide prevents cells from using oxygen to make energy molecules.

The cyanide ion, CN-, binds to the iron atom in cytochrome C oxidase in the mitochondria of cells. It acts as an irreversible enzyme inhibitor, preventing cytochrome C oxidase from doing its job, which is to transport electrons to oxygen in the electron transport chain of aerobic cellular respiration. Now unable to use oxygen, the mitochondria can't produce the energy carrier adenosine triphosphate (ATP). Tissues that require this form of energy, such as heart, muscle cells, and nerve cells, quickly expend all their energy and start to die. When a large enough number of critical cells die, you expire as well. Death usually results from respiratory or heart failure.

Immediate aymptoms include headaches, nausea and vomiting, dizziness, lack of coordination, and rapid heart rate. Long exposure symptoms include unconsciousness, convulsions, respiratory failure, coma and death.

A person exposed to cyanide may have cherry-red skin from high oxygen levels, or dark blue coloring, from Prussian blue (iron-binding to the cyanide ion). In addition to this, skin and body fluids may give off an almond odor.

The antidotes for cyanide include sodium nitrite, hydroxocobalamin, and sodium thiosulfate.

A high dose of inhaled cyanide is lethal too quickly for any treatment to take effect, but ingested cyanide or lower doses of inhaled cyanide may be countered by administering antidotes that detoxify cyanide or bind to it. For example, hydroxocobalamin, natural vitamin B12, reacts with cyanide to form cyanocobalamin, which leaves the body in urine.

These antidotes are administrated via injection, or IV infusion.

Cyanide is actually a lot more common than you'd think. It's in pesticides, fumigants, plastics, and electroplating, among other things. However, not all cyanide are so poisonous. Sodium cyanide (NaCN), potassium cyanide (KCN), hydrogen cyanide (HCN), and cyanogen chloride (CNCl) are lethal, but thousands of compounds called nitriles contain the cyanide group, yet aren't as toxic. They still aren't terribly good for you, so I wouldn't go around ingesting other cyanide compounds, but they're not quite as dangerous as the lethal kind.

Thank you for reading, have a lovely day :)

[hibiscus-misery-pills]

“Time for yourself.”

[Gender] — Female! Reader

[Warning] — Anxiety (Mild), depression (Slight), nothing much the rest is fluff.

[Synopsis] — Reader takes time for their self since the staff refuse to let reader bed rot, and they bring along their feline friend who knows how to cheer reader up.

[Word Count] —

[Author Note] — This idea is based off the outfits I see on Pinterest, also the outfits pics aren’t mines, unfortunately I don’t know the actual person who put the fit together so shout out to them. But I’m doing my face routine and I also like makeup so, I’m throwing these ideas in one plot, also if you want a male version just let me know in the comments, enjoy the story! (Also this is Imposter AU)

[P.S] — This is the outfit that inspired me to write this fic.

♡︎♡︎♡︎♡︎♡︎♡︎♡︎♡︎♡︎♡︎♡︎♡︎♡︎♡︎♡︎♡︎♡︎♡︎♡︎♡︎♡︎♡︎♡︎♡︎♡︎

It was another day in Twisted Wonderland, and you had decided to stay in bed, just lounging with Grim snuggled by your side. The ceiling fan spun lazily overhead. However, some of the staff members, particularly Crewel and Trein, disapproved of your plan to do nothing all day. Their disapproval was clear when you heard their familiar footsteps approaching your room.

The door swung open gently with a knock, and Crewel and Trein entered. You weren’t sure how they managed to convince you to get up, but before you knew it, you were on your feet. Trein informed you, "We’ll swing by and pick you up around 5," before they left. Despite being thrust into this unfamiliar world, it wasn’t entirely unkind. Remarkably, your bookbag had arrived with you and functioned as a portal for transporting things from your world. Ramshackle had been revamped by Crowley, and while it felt more homely, it still wasn’t quite comforting. The beige wallpaper with its floral design was calming, though, and the white vanity, along with wardrobes and closets from Crewel, added a touch of familiarity.

Your belongings had made the transition as well, including your electronics. They now had infinite battery life but couldn’t connect to social media or make calls. Sitting at your vanity, you decided to do your makeup, playing your favorite music through your tablet. The window’s semi-circle area was large enough to accommodate both your vanity and desk. From your vanity, you faced the front of Ramshackle, which was visible through the semi-transparent curtains. As you dusted off baking powder with a brush, you noticed someone approaching Ramshackle through the curtains. You leaned in to get a better look and saw Vil. He appeared to be in a daze, looking up at the building.

Panicking, you hid behind the vanity mirror, grateful for its size that concealed you. Vil seemed to be assessing Ramshackle before leaving a letter and gifts in the mailbox. Your heart raced as you watched him leave slowly, taking his time. As soon as he was gone, you released a sigh of relief, tears welling up in your eyes. After finishing your makeup, you dressed in your prepped outfit and matching shoes, then added a scarf for Grim to match your look. With the scarf tied around Grim’s collar, you finished your preparations and spritzed on some perfume. Just as you were about to head out, Crewel pulled up in his sports car.

As you walked out, you noticed Leona standing nearby. You hurried into the car, jumping into the passenger seat, while Leona looked on in surprise through the rearview mirror. The rest of the day passed quickly as you spent time with Crewel and Trein. They treated you warmly and spoiled you and Grim, acknowledging the trouble their students had caused. You decided to explore a small part of town with Grim, sticking close and not straying too far.

With the allowance provided by Crowley and additional funds from Crewel, you were able to buy a few special items. Among your purchases was a limited-edition jewelry set featuring a beautiful silver chain adorned with deep blue sapphires. You also bought a matching silver satin collar with a sapphire for Grim. When you returned to Ramshackle, Crewel commented on how you seemed to enjoy your time to yourself. You couldn’t help but smile, reflecting on how peaceful and content the shopping experience had made you feel.As you lay back on your bed with your new items and purse, you felt a sense of happiness and contentment. Maybe the staffs was right—you needed to take more time for yourself.

♡︎♡︎♡︎♡︎♡︎♡︎♡︎♡︎♡︎♡︎♡︎♡︎♡︎♡︎♡︎♡︎♡︎♡︎♡︎♡︎♡︎♡︎♡︎♡︎♡︎

[Author Note] — Goddamn it, I write too much, why am Im writing like i’m writing for my teachers.😭