Chaivat ToskulkaoThirayudh GlinsukonMahidol University2018-06-142018-06-141988-01-01journal of pharmacobio-dynamics. Vol.11, No.3 (1988), 191-1970386846X2-s2.0-0023897022https://repository.li.mahidol.ac.th/handle/20.500.14594/15678The possible role of hepatic lipid peroxidation and Ca2+ in enhanced hepatotoxicity of aflatoxin Bi (AFBj) by ethanol was examined along with changes in hepatic glutathione in male rats. Hepatic glutathione (GSH) was markedly decreased (43.9%) at 12 h after AFBi administration in rats treated with ethanol (4.0 g/kg BW) and AFBj (2.0 mg/kg BW) when compared to AFBj alone. At 24 h after AFBj administration, hepatic lipid peroxide levels in subcellular fractions, particularly in microsomes, were significantly increased (76.9%) in rats treated with ethanol and AFB, following the decrease in hepatic GSH content. Hepatic lipid peroxide levels returned to normal values at about 48 h after AFB, administration. Furthermore, Ca2 + in whole liver (60.9%), microsomes (83.8%) and mitochondria (51.2%) were significantly increased in the rats treated with ethanol and AFB] as compared to those rats treated with AFBj alone at 48 h after toxin administration. The increase in hepatic Ca2 + in rats treated with ethanol and AFB, was a possible consequence of the increase in hepatic lipid peroxide. These findings suggest that there is a close relationship between hepatic GSH content, lipid peroxidation and intracellular accumulation of Ca2 + . The pronounced effects on hepatic lipid peroxidation and intracellular accumulation of Ca2 + could play a role in ethanol-induced potentiation of AFBj hepatotoxicity in rats. © 1988, The Pharmaceutical Society of Japan. All rights reserved.Mahidol UniversityPharmacology, Toxicology and PharmaceuticsArticleSCOPUS10.1248/bpb1978.11.191