Enhanced hepatotoxicity induced by repeated exposure to polychlorinated biphenyls and 2,3,7,8-tetrachlorodibenzo-p-dioxin in combination in male rats  

作　　者：Yimei Wang Chunfeng Lu Zhiguo Sheng Gang Liu Ze Fu Benzhan Zhu Shuangqing Peng 

机构地区：[1]Evaluation and Research Center for Toxicology, Institute of Disease Control and Prevention, Academy of Military Medical Sciences, Beijing 100071, China [2]State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Beijing 100085, China [3]Department of Pharmacology, Basic Medical College, Jiamusi University, Jiamusi 154007, China

出　　处：《Journal of Environmental Sciences》2011年第1期119-124,共6页环境科学学报（英文版）

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)

摘　　要：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.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.

关 键 词：2 3 7 8-tetrachlorodibenzo-p-dioxin polychlorinated biphenyls combined exposure HEPATOTOXICITY 

分 类 号：X132[环境科学与工程—环境科学] Q132.1[生物学—普通生物学]