Molecular injury to mitochondria produced by ethanol and acetaldehyde

Mitochondria from ethanol fed rats display reductions in a) ability to oxidize various substrates; b) energy production with NAD⁺ dependent substrates; c) energy utilization (Ca²⁺ uptake); d) activity of several enzymes (cytochrome oxidase, succinic dehydrogenase, α glycerophosphate oxidase); and e) decreased content of cytochromes. There is no change in mitochondrial yield or concentration in rats fed ethanol chronically. The acceleration of ethanol oxidation induced by chronic ethanol feeding is not explained by increases in ''mitochondrial activity,'' capacity of shuttles for the transport of reducing equivalents into the mitochondria, or alcohol dehydrogenase activity. Other factors, including pathways unrelated to alcohol dehydrogenase or altered regulation of mitochondrial function in vivo, may be involved.