The main function of the Mitochondria

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    Energy conversion

    Mitochondria are the site of oxidative metabolism in eukaryotes, and the place where carbohydrates, fats and amino acids are finally oxidized to release energy. The common pathway of final oxidation that mitochondria is responsible for is the tricarboxylic acid cycle and oxidative phosphorylation, which correspond to the second and third stages of aerobic respiration, respectively. The glycolysis completed in the cytoplasmic matrix and the tricarboxylic acid cycle completed in the mitochondrial matrix will produce reduced nicotinarnide adenine dinucleotide (NADH) and reduced flavin adenine dinucleotide Acid (reduced flavin adenosine dinucleotide, FADH2) and other high-energy molecules, and the role of this step of oxidative phosphorylation is to use these substances to reduce oxygen to release energy to synthesize ATP. In the process of aerobic respiration, 1 molecule of glucose releases energy through glycolysis, tricarboxylic acid cycle and oxidative phosphorylation, which can produce 30 to 32 molecules of ATP (considering that NADH may need to consume 2 molecules of ATP to transport NADH into mitochondria) . If the cell's environment is hypoxic, it will switch to anaerobic respiration. At this time, pyruvate produced by glycolysis no longer enters the tricarboxylic acid cycle in the mitochondria, but continues to react in the cytoplasmic matrix (reduced by NADH into fermentation products such as ethanol or lactic acid), but does not produce ATP. Therefore, in the process of anaerobic respiration, 1 molecule of glucose can only produce 2 molecules of ATP in the first stage.

     

    Tricarboxylic acid cycle

    Each molecule of pyruvate produced in glycolysis will be actively transported across the mitochondrial membrane. After entering the mitochondrial matrix, pyruvate will be oxidized and combined with coenzyme A to produce CO2, reduced coenzyme I and acetyl-coenzyme A. Acetyl-CoA is the primary substrate of the Krebs cycle (also known as the "Citrate Cycle" or "Krebs Cycle"). The enzymes involved in this cycle are free in the mitochondrial matrix except for the succinate dehydrogenase located in the inner mitochondrial membrane. In the tricarboxylic acid cycle, each molecule of acetyl-CoA is oxidized, and at the same time, reduced cofactors (including 3 molecules of NADH and 1 molecule of FADH2) and 1 molecule of guanosine triphosphate (GTP) are produced to initiate the electron transport chain.

     

    Oxidative phosphorylation

    NADH and FADH2 and other reducing molecules (the reducing equivalent in the cytoplasmic matrix can enter the electron transport chain from the malate-aspartate shuttle system composed of antiporters or through the glycerol phosphate shuttle) in the electron transport chain After a few steps of reactions, oxygen is finally reduced and energy is released. Part of the energy is used to generate ATP, and the rest is lost as heat energy. Enzyme complexes on the inner mitochondrial membrane (NADH-ubiquinone reductase, ubiquinone-cytochrome c reductase, cytochrome c oxidase) use the energy released during the process to pump protons into the mitochondrial membrane space against the concentration gradient. Although this process is highly efficient, there are still a small amount of electrons that will reduce oxygen prematurely and form reactive oxygen species (ROS) such as superoxide. These substances can cause oxidative stress and degrade mitochondrial performance.

    When protons are pumped into the mitochondrial membrane space, an electrochemical gradient is established on both sides of the mitochondrial inner membrane, and the protons will have a tendency to diffuse along the concentration gradient. The only diffusion channel for protons is ATP synthase (respiratory chain complex V). When protons return to the mitochondrial matrix from the membrane space through the complex, the potential energy is used by ATP synthase to synthesize ADP and phosphate into ATP. This process is called "chemical infiltration", which is a kind of assisted diffusion. Peter Mitchell won the Nobel Prize in 1978 for proposing this hypothesis. In 1997, Nobel Prize winners Paul Boyer and John Wacker clarified the mechanism of ATP synthase.

     

    Store calcium ions

    Mitochondria can store calcium ions, and can cooperate with structures such as endoplasmic reticulum and extracellular matrix to control the dynamic balance of calcium ion concentration in cells. The ability of mitochondria to quickly absorb calcium ions makes it a buffer for calcium ions in the cell. Driven by the membrane potential of the inner mitochondrial membrane, calcium ions can be transported into the mitochondrial matrix by unidirectional transporters that exist in the inner mitochondrial membrane; the excretion of the mitochondrial matrix requires the assistance of sodium-calcium exchange protein or calcium-induced calcium release (calcium -induced-calcium-release, CICR) mechanism. When calcium ions are released, it will cause a "calcium wave" accompanied by a large change in membrane potential, which can activate certain second messenger system proteins to coordinate the release of neurotransmitters in synapses and hormones in endocrine cells. secretion. Mitochondria are also involved in calcium ion signal transduction during apoptosis.

     

    Other functions

    In addition to the main functions of synthesizing ATP to provide energy for cells, mitochondria also undertake many other physiological functions.

    ·Regulate membrane potential and control programmed cell death: When the contact site between the inner mitochondrial membrane and the outer membrane is produced by hexokinase (cytoplasmic matrix protein), peripheral benzodiazepine receptors and voltage-dependent anion channels (outer mitochondrial membrane protein). ), creatine kinase (mitochondrial membrane gap protein), ADP-ATP carrier (mitochondrial inner membrane protein) and cyclophilin D (mitochondrial matrix protein) and other proteins composed of the permeability transition channel (PT channel), will make The permeability of the inner mitochondrial membrane is increased, causing the dissipation of the mitochondrial transmembrane potential, which leads to cell apoptosis. The increased permeability of the mitochondrial membrane can also release molecules such as apoptosis-inducing factor (AIF) into the cytoplasmic matrix and destroy the cell structure.

    · Regulation of cell proliferation and cell metabolism;

    ·Synthesis of cholesterol and certain heme.

    Certain functions of mitochondria can only be displayed in specific tissue cells. For example, only the mitochondria in liver cells have the function of detoxifying the poison caused by ammonia (a waste product produced in the process of protein metabolism).

     

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