Abstract
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 ΔΨm and mitochondrial permeability transition [MPT]) are now recognized as a key step in apoptosis. In recent studies, including ours, the MPT 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.
| Original language | English |
|---|---|
| Pages (from-to) | 487-491 |
| Number of pages | 5 |
| Journal | Free Radical Biology and Medicine |
| Volume | 32 |
| Issue number | 6 |
| DOIs | |
| Publication status | Published - 2002 Mar 15 |
| Externally published | Yes |
Keywords
- Apoptosis
- Cytochrome c
- Free radicals
- Glutathione
- Mitochondria
- Mitochondrial permeability transition
- Oxidative stress
ASJC Scopus subject areas
- Biochemistry
- Physiology (medical)