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首页> 外文期刊>International Journal of Environmental Research and Public Health >Aniline Induces Oxidative Stress and Apoptosis of Primary Cultured Hepatocytes
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Aniline Induces Oxidative Stress and Apoptosis of Primary Cultured Hepatocytes

机译：苯胺诱导原代培养的肝细胞氧化应激和凋亡

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The toxicity and carcinogenicity of aniline in humans and animals have been well documented. However, the molecular mechanism involved in aniline-induced liver toxicity and carcinogenesis remains unclear. In our research, primary cultured hepatocytes were exposed to aniline (0, 1.25, 2.50, 5.0 and 10.0 μg/mL) for 24 h in the presence or absence of N -acetyl- l -cysteine (NAC). Levels of reactive oxygen species (ROS), malondialdehyde (MDA), and glutathione (GSH), activities of superoxide dismutase (SOD) and catalase (CAT), mitochondrial membrane potential, DNA damage, cell viability, and apoptosis were detected. Levels of ROS and MDA were significantly increased and levels of GSH and CAT, activity of SOD, and mitochondrial membrane potential in hepatocytes were significantly decreased by aniline compared with the negative control group. The tail moment and DNA content of the tail in exposed groups were significantly higher than those in the negative control group. Cell viability was reduced and apoptotic death was induced by aniline in a concentration-dependent manner. The phenomena of ROS generation, oxidative damage, loss of mitochondrial membrane potential, DNA damage and apoptosis could be prevented if ROS inhibitor NAC was added. ROS generation is involved in the loss of mitochondrial membrane potential and DNA injury, which may play a role in aniline-induced apoptosis in hepatocytes. Our study provides insight into the mechanism of aniline-induced toxicity and apoptosis of hepatocytes.
机译：苯胺对人和动物的毒性和致癌性已得到充分证明。但是，涉及苯胺诱导的肝毒性和致癌作用的分子机制仍不清楚。在我们的研究中，在存在或不存在N-乙酰-1-半胱氨酸（NAC）的情况下，将原代培养的肝细胞暴露于苯胺（0、1.25、2.50、5.0和10.0μg/ mL）24小时。检测了活性氧（ROS），丙二醛（MDA）和谷胱甘肽（GSH）的水平，超氧化物歧化酶（SOD）和过氧化氢酶（CAT）的活性，线粒体膜电位，DNA损伤，细胞活力和细胞凋亡。与阴性对照组相比，苯胺显着降低了ROS和MDA的水平，并且苯胺显着降低了肝细胞中GSH和CAT的水平，SOD活性以及线粒体膜电位。暴露组的尾巴力矩和尾巴DNA含量明显高于阴性对照组。细胞活力降低，并且苯胺以浓度依赖性方式诱导细胞凋亡死亡。加入ROS抑制剂NAC可以预防ROS的产生，氧化损伤，线粒体膜电位丧失，DNA损伤和凋亡的现象。 ROS的产生与线粒体膜电位的丧失和DNA损伤有关，这可能在苯胺诱导的肝细胞凋亡中起作用。我们的研究提供了对苯胺诱导的毒性和肝细胞凋亡机制的见解。

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