2,3,7,8-Tetrachlorodibenzo-p-dioxin （TCDD） and polychlorinated biphenyls （PCBs） are among persistent polyhalogenated aromatic hydrocarbons that exist as complex mixtures in the environment worldwide. The present s...2,3,7,8-Tetrachlorodibenzo-p-dioxin （TCDD） and polychlorinated biphenyls （PCBs） are among persistent polyhalogenated aromatic hydrocarbons that exist as complex mixtures in the environment worldwide. The present study was attempted to investigate the hepatotoxicity following repeated exposure to TCDD and PCBs in combination in male rats, and to reveal the involvement of potential mechanisms. Male Sprague-Dawley rats were exposed to TCDD （10 Ixg/kg） and Aroclor 1254 （10 mg/kg, a representative mixture of PCBs） alone or in combination by intragastric administration. After 12-day exposure, all treatments produced significant hepatotoxicity as characterized by changes of plasma biochemistry and histopathological changes. These effects were more prominent in the combined group. Furthermore, all treatments induced hepatic cytochrome P450 1A1 （CYP1A1） expression, and the maximal level of CYP1A1 expression was observed in the combined group, as in the case of the most severe hepatotoxicity evoked by the combined exposure. These findings indicated that the hepatotoxicity induced by TCDD and Aroclor 1254 might be ascribed to the high expression of hepatic CYP1A1. The present study demonstrates the enhanced hepatotoxicity after exposure to TCDD and PCBs in combination in rats.展开更多
基金supported by the National Basic Research Program (973) of China (No.2011CB503803)partly financed by the State Key Laboratory of Environmental Chemistry and Ecotoxicology,Research Center for Eco-Environmental Sciences,Chinese Academy of Sciences (No.KF2008-20)
文摘2,3,7,8-Tetrachlorodibenzo-p-dioxin （TCDD） and polychlorinated biphenyls （PCBs） are among persistent polyhalogenated aromatic hydrocarbons that exist as complex mixtures in the environment worldwide. The present study was attempted to investigate the hepatotoxicity following repeated exposure to TCDD and PCBs in combination in male rats, and to reveal the involvement of potential mechanisms. Male Sprague-Dawley rats were exposed to TCDD （10 Ixg/kg） and Aroclor 1254 （10 mg/kg, a representative mixture of PCBs） alone or in combination by intragastric administration. After 12-day exposure, all treatments produced significant hepatotoxicity as characterized by changes of plasma biochemistry and histopathological changes. These effects were more prominent in the combined group. Furthermore, all treatments induced hepatic cytochrome P450 1A1 （CYP1A1） expression, and the maximal level of CYP1A1 expression was observed in the combined group, as in the case of the most severe hepatotoxicity evoked by the combined exposure. These findings indicated that the hepatotoxicity induced by TCDD and Aroclor 1254 might be ascribed to the high expression of hepatic CYP1A1. The present study demonstrates the enhanced hepatotoxicity after exposure to TCDD and PCBs in combination in rats.
