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Fig. 1 | Military Medical Research

Fig. 1

From: Potential therapy strategy: targeting mitochondrial dysfunction in sepsis

Fig. 1

Electron transport chain (ETC) components and its function. NADH and FADH2 are produced from the intermediary metabolism of glucose (carbohydrate), lipid (fat), and glutamine (protein); and they donate electrons to complex I (NADH-ubiquinone oxidoreductase) and complex II (succinate-ubiquinone oxidoreductase). These electrons are passed sequentially to coenzyme Q (or ubiquinone) to form CoQH2, and then transfers its electron to complex III (ubiquinol-cytochrome C oxidase reductase). Complex III transfers electrons to cytochrome C, which pass them to complex IV (cytochrome C oxidase or COX). At last complex IV donates an electron to O2 to produce H2O. The energy liberated by the flow of electrons is used by complexes I, III, and IV to pump protons (H+) out of the mitochondrial inner membrane (IM) into the intermembrane space. This proton gradient generates the mitochondrial membrane potential that is coupled to ATP (Adenosin triiphosphate) synthesis by complex V (ATPase) from ADP (adenosin diphosphate) and inorganic phosphate (Pi). OM. Outer membrane; NADH. Oxidized nicotinamide adenine dinucleotide; NAD+. Reduced nicotinamide adenine dinucleotide; FADH. Oxidized flavin adenine dinucleotide; FAD+. Reduced flavin adenine dinucleotide

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