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首页> 外文期刊>Journal of applied toxicology >Induction of hepatotoxicity by sanguinarine is associated with oxidation of protein thiols and disturbance of mitochondrial respiration.
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Induction of hepatotoxicity by sanguinarine is associated with oxidation of protein thiols and disturbance of mitochondrial respiration.

机译：血红素碱诱导的肝毒性与蛋白硫醇的氧化和线粒体呼吸的紊乱有关。

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摘要

Sanguinarine (SANG) has been suggested to be one of the principle constituents responsible for the toxicity of Argemone mexicana seed oil. In this study, we focused on the possible mechanism of SANG-induced hepatotoxicity. The serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactate dehydrogenase (LDH) activities, hepatic vacuolization, lipid accumulation and lipid peroxidation of the liver were increased, and triglyceride (TG) was decreased in SANG-treated mice (10 mg kg(-1) i.p.), indicating damage to the liver. SANG induced cell death and DNA fragmentation, in a concentration- (0-30 microm) and time-dependent (0-24 h) manner, and the cytotoxicity of SANG (15 microm) was accompanied by an increase in reactive oxygen species and a lessening in protein thiol content; these outcomes were reversed by glutathione, N-acetyl-l-cysteine and 1,4-dithiothretol, and slightly improved by other antioxidants in hepatocytes. SANG can affect the function of mitochondria, leading to the depletion of the mitochondrial membrane potential and adenosine 5'-triphosphate content of hepatocytes. SANG caused an uncoupling effect of the respiratory chain at lower concentrations, but inhibited the respiratory chain at higher concentrations in mitochondria isolated from rat liver. In conclusion, the data suggest that SANG is a liver toxin that induces cytotoxicity in liver cells, possibly through oxidation of protein thiols, resulting in oxidative stress on the cells and disturbance of mitochondrial function. Copyright (c) 2008 John Wiley & Sons, Ltd.
机译：有人建议将Sanguinarine（SANG）作为负责墨西哥精油种子油毒性的主要成分之一。在这项研究中，我们集中于桑格诱导的肝毒性的可能机制。在SANG处理的小鼠中，血清天冬氨酸转氨酶（AST），丙氨酸转氨酶（ALT）和乳酸脱氢酶（LDH）活性，肝空泡，脂质积累和脂质过氧化增加，甘油三酸酯（TG）降低（10） mg kg（-1）ip），表明对肝脏有损害。 SANG以浓度（0-30 microm）和时间依赖性（0-24 h）的方式诱导细胞死亡和DNA断裂，SANG的细胞毒性（15 microm）伴随着活性氧的增加和减少蛋白质硫醇含量;谷胱甘肽，N-乙酰基-1-半胱氨酸和1,4-二硫苏糖醇逆转了这些结果，肝细胞中的其他抗氧化剂略微改善了这些结果。 SANG可以影响线粒体的功能，导致线粒体膜电位的消耗和肝细胞5'-三磷酸腺苷含量的降低。 SANG引起较低浓度的呼吸链的解偶联作用，但从大鼠肝脏分离的线粒体中较高浓度的呼吸链却受到抑制。总之，数据表明SANG是一种肝毒素，可能通过蛋白质硫醇的氧化诱导肝细胞的细胞毒性，从而导致细胞氧化应激和线粒体功能紊乱。版权所有（c）2008 John Wiley＆Sons，Ltd.

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