Mitochondrial glutathione and chemically induced stress including ethanol.
The mechanisms of alcohol toxicity as related to mitochondrial dysfunction and the glutathione-dependent protective systems are reviewed. The pathophysiology of ethanol-induced liver damage is defined in terms of an early phase and a late phase. CYP2E1 dependent toxicity appears closely related to oxidative stress injury with possible roles of peroxynitrite, TNFalpha, protein adducts, and enhanced protein expression. Modulation of mitochondrial glutathione affects mitochondrial function and cell survival with superoxide and hydrogen peroxide generation being crucial to mitochondrial membrane permeability transition and apoptosis.
Reed
Donald J
DJ
Department of Biochemistry and Biophysics, 2011 ALS, Oregon State University, Corvallis, Oregon 97331, USA. Donald.reed@orst.edu
D000818:Animals; D000431:Ethanol / Q000378:metabolism* / Q000633:toxicity; D005978:Glutathione / Q000378:metabolism*; D006801:Humans; D008930:Mitochondria, Liver / Q000187:drug effects / Q000378:metabolism*; D013312:Stress, Physiological / Q000139:chemically induced / Q000378:metabolism*
D000431:Ethanol; D005978:Glutathione