[Mechanism of auto-oscillations in mitochondria based on modulations of succinate dehydrogenase activity].
The viewpoint is substantiated according to which pulsations of proton and electron flow pressure in the respiratory chain serve as a generator of stable high-amplitude self-oscillations in mitochondria (MCH) due to reversible inhibition of succinate dehydrogenase (SDG) by oxalacetic acid (OAA). Damage of coupling and membrane permeability increase are initiated at high rate of respiration under hypotonic media and cation loading. Then slow restoration of permeability occurs under low rate respiration which is completed by its rise that closes the cycle. The latter is due to autocatalytic release of OAA from SDG in which reduced pyridine nucleotides (PNH) participate. Phenomenological model of oscillating state of MCH is proposed consisting of two common differential equations describing changes of respiration and PN reduction rates. Under realistic values of parameters the model predicts oscillations of respiration intensity and PNH level whose shape correlates well with the experimental data. The presented model is the only mathematical description of concrete experimental oscillations in mitochondria.
D004579:Electron Transport; D008928:Mitochondria / Q000201:enzymology / Q000378:metabolism*; D008954:Models, Biological; D010071:Oxaloacetates / Q000378:metabolism; D010084:Oxidation-Reduction; D010101:Oxygen Consumption; D011725:Pyridines / Q000378:metabolism; D013385:Succinate Dehydrogenase / Q000037:antagonists & inhibitors / Q000378:metabolism*
D010071:Oxaloacetates; D011725:Pyridines; D013385:Succinate Dehydrogenase
Mekhanizm avtokolebaniĭ v mitokhondriiakh, osnovannyĭ na moduliatsii aktivnosti suktsinatdegidrogenazy.