The Role of the Keap1/Nrf2 Pathway in the Cellular Response to Methylmercury. (26th June 2013)

• Record Type: Journal Article
• Authors: Kumagai, Yoshito; Kanda, Hironori; Shinkai, Yasuhiro; Toyama, Takashi
• Other Names: Kwak Mi-Kyoung Academic Editor.
• Is Part Of: Oxidative medicine and cellular longevity. Volume 2013(2013)
• Publication Date: 2013-06-26
• Subjects: Oxidative stress -- Periodicals; Cells -- Aging -- Periodicals; Cells -- Aging; Oxidative stress; Oxidative Stress -- Periodicals; Cell Aging -- Periodicals; Periodicals; 611.0181
• DOI: 10.1155/2013/848279
• Languages: English
• ISSNs: 1942-0900

Abstract

Abstract : 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.