Induction of reactive oxygen species by bisphenol A and abrogation of bisphenol A-induced cell injury by DJ-1
Induction of reactive oxygen species by bisphenol A and abrogation of bisphenol A-induced cell injury by DJ-1
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DOI：
10.1093/toxsci/kfi278
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发表时间：
2005-11-01
影响因子：
3.8
通讯作者：
Ariga, H
中科院分区：
文献类型：
--
作者：
Ooe, H;Taira, T;Ariga, H
DJ-1首先被鉴定为一种激活的ras依赖性癌基因。DJ-1与男性生育能力有关，暴露于一些生殖毒物后，其在精子中的表达会减少。DJ-1与人类家族性帕金森病（PD）的发病有关，并被发现通过消除活性氧（ROS）具有抗氧化损伤的活性。在这项研究中，我们通过双酚A （BPA）的管理研究了DJ-1在氧化应激中的作用，双酚A在啮齿类动物、雄性小鼠和培养细胞中诱导氧化应激。在雄性小鼠中，我们发现BPA显著增加了DJ-1在精子和大脑中的表达水平。在培养的Neuro2a和GC1细胞中，我们发现BPA诱导ROS产生，并显著损害线粒体功能，同时升高DJ-1的表达和氧化。研究发现，DJ-1在线粒体定位后能够维持复合物I的活性，抵抗bpa诱导的氧化应激。结果表明，DJ-1在线粒体损伤诱导的细胞死亡中起预防作用。
DJ-1 was first identified as an activated ras-dependent oncogene. DJ-1 is related to male fertility, and its expression in sperm decreases in response to exposure to a number of reproductive toxicants. DJ-1 has been associated with the onset of familial Parkinson's disease (PD) in humans, and has been found to have activity against oxidative damage by eliminating reactive oxygen species (ROS). In this study, we investigated the role of DJ-1 in oxidative stresses by administration of bisphenol A (BPA), which has been reported to induce oxidative stress in rodents, to male mice and cultured cells. In male mice, we found that BPA significantly increased the expression level of DJ-1 in the sperm and brain. In cultured Neuro2a and GC1 cells, we found that BPA induced ROS production and significantly compromised mitochondrial function concomitant with elevated expression and oxidization of DJ-1. DJ-1 was found to maintain the complex I activity against BPA-induced oxidative stress after the localization in mitochondria. The results showed that DJ-1 plays a role in the prevention of mitochondrial injury-induced cell death.