Dietary choline restriction causes complex I dysfunction and increased H2O2 generation in liver mitochondria.

from normal rats, and the NADH-specific yield of H2O2 is course of complex I alteration correlated with the time course of increased by at least 2.5-fold. These findings suggest an lipid compositional changes as indicated by mass spectrometric explanation for the rapid onset of oxidative stress and analysis of phosphatidylcholine (PC) and consistent with energy compromise in the choline deficiency model of previously published data. Finally, it was found that lipids hepatocellular carcinoma and indicate that dietary choline extracted from CDAA mitochondria can impair NADH-dehywithdrawal may be a useful paradigm for the study of drogenase activity when reconstituted with protein extracted mitochondrial pathophysiology in carcinogenesis. from normal mitochondria. These data provide a theoretical context for discussing oxidative damage in the CDAA model of hepatocellular carcinoma, and provide a striking example