Beneficial effect of nitric oxide synthase inhibitor on hepatotoxicity induced by allyl alcohol
Beneficial effect of nitric oxide synthase inhibitor on hepatotoxicity induced by allyl alcohol
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DOI：
10.1002/jbt.10008
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发表时间：
2001-01-01
影响因子：
3.6
通讯作者：
Al-Bekairi, AM
中科院分区：
文献类型：
--
作者：
Alam, K;Nagi, MN;Al-Bekairi, AM
通过测定血清ALT、AST活性和组织病理学检查，观察诱导型一氧化氮合酶（iNOS）抑制剂氨基胍（aminoguanidine，AM）对烯丙醇肝损伤的影响。当氨基胍（50-300 mg/kg，i. p.）在毒性剂量的烯丙醇（75穆尔/kg，i. p.）之前30分钟给予小鼠，观察到与肝损伤相关的显著变化。在氨基胍的存在下，ALT和AST酶的水平显着降低。用300 mg/kg氨基胍预处理动物时，由烯丙醇毒性引起的肝坏死的所有症状几乎完全消失。在用300 mg/kg氨基胍预处理的小鼠中，由于烯丙醇代谢导致的肝脏谷胱甘肽消耗极小。结果发现，抑制毒性不是由于烯丙醇代谢的改变，因为氨基胍不影响乙醇脱氢酶活性在体内和体外。(C)John Wiley & Sons，Inc.
The effect of aminoguanidine (a selective inhibitor of inducible nitric oxide synthase) on allyl alcohol-induced liver injury was assessed by the measurement of serum ALT and AST activities and histopathological examination. When aminoguanidine (50-300 mg/kg, i.p.) was administered to mice 30 min before a toxic dose of allyl alcohol (75 muL/kg, i.p.), significant changes related to liver injury were observed. In the presence of aminoguanidine the level of ALT and AST enzymes were significantly decreased. All symptoms of liver necrosis produced by allyl alcohol toxicity almost completely disappeared when animals were pretreated with aminoguanidine at 300 mg/kg. Depletion of hepatic glutathione as a consequence of allyl alcohol metabolism was minimal in mice pretreated with aminoguanidine at 300 mg/kg. It was found that the inhibition of toxicity was not due to alteration in allyl alcohol metabolism since aminoguanidine did not effect alcohol dehydrogenase activity both in vivo and in vitro. (C) 2001 John Wiley & Sons, Inc.