Acetaminophen hepatotoxicity in vivo is not accompanied by oxidant stress.
Acetaminophen hepatotoxicity in vivo is not accompanied by oxidant stress.
复制标题
对乙酰氨基酚的体内肝毒性不伴随氧化应激。
DOI：
10.1016/0006-291x(85)91879-0
复制
发表时间：
1985
影响因子：
3.1
通讯作者：
Mitchell,JR
中科院分区：
文献类型：
--
作者：
Smith,CV;Mitchell,JR
在Fischer 344大鼠中，肝毒性剂量的对乙酰氨基酚不增加氧化谷胱甘肽的胆汁外流。双(2-氯乙基)-N-亚硝脲对肝脏谷胱甘肽还原酶有73%的抑制作用，但不能增强对乙酰氨基酚的肝毒性，也不能增加对乙酰氨基酚引起的氧化谷胱甘肽的胆汁流出。对乙酰氨基酚不能耗尽肝脏蛋白质硫醇含量。在对乙酰氨基酚诱导的肝毒性中，氧化应激机制由活性氧物种或由反应性代谢物的直接氧化作用所介导的提议是未经证实的，也不太可能。
Hepatotoxic doses of acetaminophen in Fischer 344 rats did not increase biliary efflux of oxidized glutathione. Pretreatment of the animals with bis(2-chloroethyl)-N-nitrosourea inhibited hepatic glutathione reductase by 73 percent but did not potentiate the hepatotoxicity of acetaminophen and did not produce an increase in biliary efflux of oxidized glutathione in response to acetaminophen. Hepatic protein thiol content was not depleted by acetaminophen. A proposed role for oxidant stress mechanisms mediated either by reactive oxygen species or by the direct oxidant action of a reactive metabolite in acetaminophen-induced hepatotoxicity is unsubstantiated and unlikely.