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 |
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Keywords
- Apoptosis
- Cytochrome c
- Free radicals
- Glutathione
- Mitochondria
- Mitochondrial permeability transition
- Oxidative stress
ASJC Scopus subject areas
- Medicine(all)
- Toxicology
- Clinical Biochemistry
Cite this
Role of mitochondria in alcoholic liver injury. / Adachi, Masayuki; Ishii, Hiromasa.
In: Free Radical Biology and Medicine, Vol. 32, No. 6, 15.03.2002, p. 487-491.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Role of mitochondria in alcoholic liver injury
AU - Adachi, Masayuki
AU - Ishii, Hiromasa
PY - 2002/3/15
Y1 - 2002/3/15
N2 - 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.
AB - 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.
KW - Apoptosis
KW - Cytochrome c
KW - Free radicals
KW - Glutathione
KW - Mitochondria
KW - Mitochondrial permeability transition
KW - Oxidative stress
UR - http://www.scopus.com/inward/record.url?scp=0037087202&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0037087202&partnerID=8YFLogxK
U2 - 10.1016/S0891-5849(02)00740-2
DO - 10.1016/S0891-5849(02)00740-2
M3 - Article
VL - 32
SP - 487
EP - 491
JO - Free Radical Biology and Medicine
JF - Free Radical Biology and Medicine
SN - 0891-5849
IS - 6
ER -