Production of lipid hydroperoxides and depletion of reduced glutathione in liver mitochondria after acute ethanol administration to rats.
It has been found that acute ethanol (EtOH) intoxication to rats caused approximately 40% depletion of mitochondrial reduced glutathione (GSH). A GSH reduction of similar extent was also observed after the administration to rats of buthionine sulfoximine (BSO), a specific inhibitor of GSH synthesis. The combined treatment of EtOH plus BSO induced a further mitochondrial GSH decrease up to 70% with respect to control. The presence of lipid hydroperoxides in the mitochondrial membrane was observed whenever an additional oxidative stress was associated to a condition of GSH depletion as in the case of EtOH or EtOH plus BSO. Under these conditions a severe derangement in mitochondrial oxidative functions occurred.
Trenti
T
T
Clinical Pharmacology and Toxicology Institute, University of Modena, Italy.
Sternieri
E
E
Ceccarelli
D
D
Gallesi
D
D
Masini
A
A
D000818:Animals; D019328:Buthionine Sulfoximine; D000431:Ethanol / Q000633:toxicity*; D005260:Female; D005978:Glutathione / Q000378:metabolism*; D008054:Lipid Peroxides / Q000378:metabolism*; D008717:Methionine Sulfoximine / Q000031:analogs & derivatives / Q000494:pharmacology; D008930:Mitochondria, Liver / Q000187:drug effects* / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley
D008054:Lipid Peroxides; D008717:Methionine Sulfoximine; D000431:Ethanol; D019328:Buthionine Sulfoximine; D005978:Glutathione