Journal
FREE RADICAL BIOLOGY AND MEDICINE
Volume 32, Issue 6, Pages 487-491Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/S0891-5849(02)00740-2
Keywords
oxidative stress; mitochondria; apoptosis; mitochondrial permeability transition; glutathione; cytochrome c; free radicals
Ask authors/readers for more resources
Oxidative stress and oxygen-derived free radicals are well known to play an important role in the pathogenesis of ethanol-associated liver injury. Active oxidants produced during ethanol metabolism induce mitochondrial membrane depolarization and permeability changes in cultured hepatocytes. These mitochondrial alterations (loss of DeltaPsim and mitochondrial permeability transition [MPT]) are now recognized as a key step in apoptosis. In recent studies, including ours, the NIPT has been identified as a key step for the induction of mitochondrial cytochrome c release and caspase activation by ethanol. In addition, chronic and/or acute ethanol modulates intracellular, especially mitochondrial, antioxidant levels, leading to the increased susceptibility to alcoholic liver injury induced by several apoptotic stimuli. In this review, we address the mechanism of mitochondrial alterations and liver injury induced by ethanol. (C) 2002 Elsevier Science Inc.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available