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首页> 外文期刊>Life sciences >Nonylphenol enhances apoptosis induced by serum deprivation in PC12 cells
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Nonylphenol enhances apoptosis induced by serum deprivation in PC12 cells

机译：壬基酚增强血清剥夺诱导的PC12细胞凋亡

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Although nonylphenol is well known as an endocrine disrupting chemical, there is little information concerning biological effect of nonylphenol. In this study, we investigated effect of nonylphenol on apoptosis induced by serum deprivation in PC 12 cells using TUNEL and DNA fragmentation assays. In addition, changes in contents of proapoptotic factors, Bad and Bax, and antiapoptotic factor, Bcl-2, and enzyme activity of caspase-3 were studied. Below 100 ng/ml of nonylphenol increased TUNEL signals, DNA fragmentation and content of proapoptotic factor, Bad as compared to those by serum deprivation without nonylphenol. Furthermore, addition of nonylphenol enhanced caspase-3 activity and Z-VAD, caspase-3 inhibitor, diminished such effect. These results indicated that below 100 ng/ml of nonylphenol enhanced apoptosis induced by serum deprivation via caspase-3 activation in PC12 cell. (C) 2004 Elsevier Inc. All rights reserved. [References: 36]
机译：尽管壬基酚是众所周知的破坏内分泌的化学物质，但是关于壬基酚的生物学作用的信息很少。在这项研究中，我们研究了壬基酚对PC 12细胞中血清剥夺诱导的凋亡的影响，使用TUNEL和DNA片段测定法。此外，还研究了促凋亡因子Bad和Bax，抗凋亡因子Bcl-2和caspase-3酶活性的变化。与没有壬基酚的血清剥夺相比，低于100 ng / ml的壬基酚会增加TUNEL信号，DNA片段化和促凋亡因子含量Bad。此外，添加壬基酚增强了caspase-3活性，而c-ase-3抑制剂Z-VAD减弱了这种作用。这些结果表明低于100ng / ml的壬基酚增强了通过在PC12细胞中通过caspase-3活化的血清剥夺诱导的凋亡。 （C）2004 Elsevier Inc.保留所有权利。 [参考：36]

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