The role of the Keap1/Nrf2 pathway in the cellular response to methylmercury.
The role of the Keap1/Nrf2 pathway in the cellular response to methylmercury.
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DOI：
10.1155/2013/848279
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发表时间：
2013
影响因子：
--
通讯作者：
Toyama T
中科院分区：
文献类型：
--
作者：
Kumagai Y;Kanda H;Shinkai Y;Toyama T
甲基汞（MeHg）是一种环境亲电试剂，可通过活性硫醇共价修饰细胞蛋白质，从而形成蛋白质加合物。虽然这种蛋白质修饰（称为S-汞化）被认为与甲基汞暴露引起的酶功能障碍和细胞损伤有关，但目前的共识是：（1）通过激活NF-E2相关因子2（Nrf 2）并结合其负调节因子Kelch样ECH相关蛋白1（Keap 1）的S-汞化，（2）Keap 1/Nrf 2通路对甲基汞毒性具有保护作用。在这篇综述中，我们介绍了我们的研究结果，并讨论了其他工作人员的观察有关的S-汞的细胞蛋白质的甲基汞和Keap 1/Nrf 2途径的重要性，在培养的细胞和小鼠对甲基汞毒性的保护。
Methylmercury (MeHg) is an environmental electrophile that covalently modifies cellular proteins with reactive thiols, resulting in the formation of protein adducts. While such protein modifications, referred to as S-mercuration, are thought to be associated with the enzyme dysfunction and cellular damage caused by MeHg exposure, the current consensus is that (1) there is a cellular response to MeHg through the activation of NF-E2-related factor 2 (Nrf2) coupled to S-mercuration of its negative regulator, Kelch-like ECH-associated protein 1 (Keap1), and (2) the Keap1/Nrf2 pathway protects against MeHg toxicity. In this review, we introduce our findings and discuss the observations of other workers concerning the S-mercuration of cellular proteins by MeHg and the importance of the Keap1/Nrf2 pathway in protection against MeHg toxicity in cultured cells and mice.
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