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活性氧在黄曲霉毒素B1诱导的培养大鼠肝细胞损伤中的作用。

Involvement of reactive oxygen species in aflatoxin B1-induced cell injury in cultured rat hepatocytes.

作者信息

Shen H M, Ong C N, Shi C Y

机构信息

Department of Community, Occupational and Family Medicine, National University of Singapore.

出版信息

Toxicology. 1995 May 5;99(1-2):115-23. doi: 10.1016/0300-483x(94)03008-p.

Abstract

The role of reactive oxygen species (ROS) in AFB1-induced cell injury was investigated using cultured rat hepatocytes. Malonaldehyde (MDA) generation and lactate dehydrogenase (LDH) release were determined as indices of lipid peroxidation and cell injury, respectively. Exposure to AFB1 for up to 72 h resulted in significantly elevated levels of LDH being released into the medium as well as the MDA generation in cultured hepatocytes. These effects were dose-dependent, indicating that AFB1 was capable of inducing oxidative damages in the cell. Further, MDA generation and LDH release were effectively inhibited by the addition of the following: (1) superoxide dismutase (500 units/ml), (2) catalase (1500 units/ml), (3) 10 mM desferrioxamine (a specific iron chelator), or (4) 260 mM dimethyl sulfoxide (a hydroxyl radical scavenger). These evidences therefore suggest that ROS, such as superoxide radicals, hydroxyl radicals and hydrogen peroxides, are involved in AFB1-induced cell injury in cultured rat hepatocytes.

摘要

利用培养的大鼠肝细胞研究了活性氧(ROS)在黄曲霉毒素B1(AFB1)诱导的细胞损伤中的作用。分别测定丙二醛(MDA)生成量和乳酸脱氢酶(LDH)释放量作为脂质过氧化和细胞损伤的指标。暴露于AFB1长达72小时导致释放到培养基中的LDH水平以及培养肝细胞中MDA生成量显著升高。这些效应呈剂量依赖性,表明AFB1能够诱导细胞中的氧化损伤。此外,添加以下物质可有效抑制MDA生成和LDH释放:(1)超氧化物歧化酶(500单位/毫升),(2)过氧化氢酶(1500单位/毫升),(3)10毫摩尔去铁胺(一种特异性铁螯合剂),或(4)260毫摩尔二甲基亚砜(一种羟自由基清除剂)。因此,这些证据表明超氧自由基、羟自由基和过氧化氢等ROS参与了AFB1诱导的培养大鼠肝细胞损伤。

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