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Review
. 2020 Jul 17;25(1):30.
doi: 10.1186/s12199-020-00868-3.

Methylmercury toxic mechanism related to protein degradation and chemokine transcription

Jin-Yong Lee  1 , Gi-Wook Hwang  2   3 , Akira Naganuma  3 , Masahiko Satoh  4
Affiliations
Review

Methylmercury toxic mechanism related to protein degradation and chemokine transcription

Jin-Yong Lee et al. Environ Health Prev Med. .

Abstract

Methylmercury is an environmental pollutant that causes neurotoxicity. Recent studies have reported that the ubiquitin-proteasome system is involved in defense against methylmercury toxicity through the degradation of proteins synthesizing the pyruvate. Mitochondrial accumulation of pyruvate can enhance methylmercury toxicity. In addition, methylmercury exposure induces several immune-related chemokines, specifically in the brain, and may cause neurotoxicity. This summary highlights several molecular mechanisms of methylmercury-induced neurotoxicity.

Keywords: Chemokines; Methylmercury; Mitochondria; Pyruvate; Ubiquitin-proteasome pathway.

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Conflict of interest statement

The authors declare that they have no competing interests.

Figures

Fig. 1
Fig. 1
The ubiquitin-proteasome system involved in methylmercury toxicity. The target proteins, Dld3 and Eno2, respectively specific to Hrt1 and Ucc1 enhance methylmercury toxicity, unless they are degraded by ubiquitin-proteasome system. E1, ubiquitin activating enzyme; E2, ubiquitin conjugating enzyme; E3, ubiquitin ligase; Ub, ubiquitin
Fig. 2
Fig. 2
The scheme of methylmercury toxic mechanism by the pyruvate transportation into mitochondria. MeHg+, methylmercury; ΔΨm, mitochondrial membrane potential; ROS, reactive oxygen species
See this image and copyright information in PMC

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