Decrease of hepatic mitochondrial glutathione and mitochondrial injury induced by 1,2-dibromoethane in the rat in vivo: effect of diethylmaleate pretreatment.
Diethylmaleate (DEM) potentiated the 1,2-dibromoethane (DBE)-induced hepatic morphological lesion in fasted male Wistar rats, as revealed by light and electron microscopy examination. The subcellular structures involved in such lesions were the mitochondria. The potentiating effect of DEM appeared to be due to enhancement of the depletion of hepatic mitochondrial glutathione (GSH) caused by DBE. DEM, however, failed to potentiate the DBE-induced release in the plasma of hepatic enzymes. The relationship between loss of mitochondrial GSH, mitochondrial injury, and the importance of the mitochondrial lesion in DBE-induced hepatotoxicity is discussed.
D000818:Animals; D015946:Ethylene Dibromide / Q000037:antagonists & inhibitors / Q000633:toxicity*; D005978:Glutathione / Q000378:metabolism*; D006842:Hydrocarbons, Brominated / Q000633:toxicity*; D008297:Male; D008298:Maleates / Q000494:pharmacology*; D008854:Microscopy, Electron; D008930:Mitochondria, Liver / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D051381:Rats; D011919:Rats, Inbred Strains; D013347:Subcellular Fractions / Q000187:drug effects / Q000378:metabolism
D006842:Hydrocarbons, Brominated; D008298:Maleates; D015946:Ethylene Dibromide; C014476:diethyl maleate; D005978:Glutathione