【摘 要】
：
目的 全氟辛烷磺酸(perfluorooctane sulfonate,PFOS),被广泛应用于工业生产领域和民用产品,但PFOS具有难降解性、生物蓄积性,因此引起沿食物链传播.肝脏是PFOS的主要靶器官.研究发现PFOS可损伤肝脏、增加肝细胞内活性氧浓度,导致肝细胞色素氧化酶、谷胱甘肽过氧化物酶和超氧化物歧化酶活性降低.但PFOS对肝脏二相代谢酶谷胱甘肽-S-转移酶(glutathione-S-
【机 构】
：
大连医科大学 大连医科大学药学院药理教研室
【出 处】
：
第十届全国药物和化学异物代谢学术会议暨第三届国际ISSX/CSSX联合学术会议
论文部分内容阅读
目的 全氟辛烷磺酸(perfluorooctane sulfonate,PFOS),被广泛应用于工业生产领域和民用产品,但PFOS具有难降解性、生物蓄积性,因此引起沿食物链传播.肝脏是PFOS的主要靶器官.研究发现PFOS可损伤肝脏、增加肝细胞内活性氧浓度,导致肝细胞色素氧化酶、谷胱甘肽过氧化物酶和超氧化物歧化酶活性降低.但PFOS对肝脏二相代谢酶谷胱甘肽-S-转移酶(glutathione-S-transferase,GST)及醌氧化还原酶(NAD (P)H quinone oxidoreductase 1,NQO1)的作用尚未见报道,因此本研究拟应用小鼠模型研究PFOS对肝脏的损伤作用及对二相代谢酶GST及NQ01的作用,为全面阐明PFOS对肝脏的作用增加新的实验依据.方法 予小鼠PFOS高、中、低剂量(7.5、15、30mg/kg/d)灌胃一周后,分别取血、肝组织等测定血AST、ALT,肝组织总抗氧化能力、GST和NQO1的活性.结果 PFOS可导致小鼠体重明显下降、血ALT及AST显著升高,提示PFOS引起了显著的肝损伤.同时,PFOS可引起肝总抗氧化能力降低,GST呈降低趋势,但无统计学意义.NQO1的活性显著升高,并呈显著的剂量相关性.结论 PFOS导致显著的肝损伤及降低肝脏总抗氧化能力的同时,具有一定的降低肝脏二相代谢酶GST、显著升高二相代谢酶NQO1的作用.
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