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Mitochondria in striatal synapses in mice with mutated Htt show an increased rate of proton leakage compared to wild type mice

The underlying mechanism is as follows: in the presence of the terminal electron acceptor -oxygen- the electron transport chain maintains oxidation of NADH to NAD + by complex I, and this NAD + is supporting dehydrogenases, including the pyruvate dehydrogenase complex

Complex I dysfunction results in substantially reduced ATP production, creating an energy deficit that directly compromises sperm motility and cellular function ( 3.4 Molecular pathway interaction networks The reproductive toxicity induced by EEDs results from complex crosstalk among oxidative stress responses, metabolic disruption, and immune system activation rather than isolated pathway effects