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首页> 外文期刊>Journal of biochemical and molecular toxicology >Characterization of Cd-induced molecular events prior to cellular damage in primary rat hepatocytes in culture: Activation of the stress activated signal protein JNK and transcription factor AP-1.
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Characterization of Cd-induced molecular events prior to cellular damage in primary rat hepatocytes in culture: Activation of the stress activated signal protein JNK and transcription factor AP-1.

机译：在培养的原代大鼠肝细胞中细胞损伤之前，镉诱导的分子事件的表征：应激激活信号蛋白JNK和转录因子AP-1的激活。

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摘要

The effect of Cadmium (Cd) on the expression of c-Jun N-terminal kinase (JNK), c-jun, and activator protein-1 (AP-1) has been investigated. We previously reported that Cd causes cell damage as indicated by increases in the cytotoxic parameters, lactate dehydrogenase and lipid peroxidation, and this damage was mediated by decreases in cellular concentration of glutathione. In the present study, we investigate the molecular events involved prior to the Cd-induced cellular toxicity and damage in primary rat hepatocytes. We propose that Cd, through the generation of reactive oxygen species (ROS) and prior to significant cellular damage, activates the stress activated signal protein JNK, regulates c-jun expression, and promotes the binding of a redox sensitive transcription factor AP-1. We show JNK activity and c-jun mRNA level significantly increased at 1 h and AP-1 DNA binding activity significantly enhanced at 3 h in the presence of 4 microM cadmium chloride. Blocking the Cd induction of JNK activity, c-jun mRNA level, and AP-1 binding activity using the antioxidants N-acetyl cysteine (10 mM) or carnosol (0.5 microg/mL) suggests a role for ROS. Blocking JNK activity and c-jun mRNA by SP600125 (20 microM), a JNK inhibitor, supports the role of JNK in transmission of signals induced by Cd.
机译：研究了镉（Cd）对c-Jun N末端激酶（JNK），c-jun和激活蛋白1（AP-1）表达的影响。我们以前曾报道过Cd会引起细胞损伤，如细胞毒性参数，乳酸脱氢酶和脂质过氧化作用的增加所表明的，而这种损伤是由谷胱甘肽细胞浓度的降低介导的。在本研究中，我们调查了Cd诱导的细胞毒性和原代大鼠肝细胞损伤之前涉及的分子事件。我们建议镉，通过产生活性氧（ROS）并在明显的细胞损伤之前，激活压力激活信号蛋白JNK，调节c-jun表达，并促进氧化还原敏感性转录因子AP-1的结合。我们显示，在存在4 microM氯化镉的情况下，JNK活性和c-jun mRNA水平在1 h显着增加，AP-1 DNA结合活性在3 h显着增强。使用抗氧化剂N-乙酰半胱氨酸（10 mM）或鼠尾草酚（0.5 microg / mL）阻断Jd活性，c-jun mRNA水平和AP-1结合活性对Cd的诱导，表明ROS的作用。通过SP600125（20 microM）（一种JNK抑制剂）阻断JNK活性和c-jun mRNA，支持JNK在Cd诱导的信号传递中的作用。

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