Methylmercury-Mediated Oxidative Stress and Activation of the Cellular Protective System.
Keap1/Nrf2 pathway
binding affinity
methylmercury
nonsense-mediated mRNA decay
oxidative stress
posttranscriptional defect
redox signaling
selenoenzyme
thiol antioxidant capacity
Journal
Antioxidants (Basel, Switzerland)
ISSN: 2076-3921
Titre abrégé: Antioxidants (Basel)
Pays: Switzerland
ID NLM: 101668981
Informations de publication
Date de publication:
16 Oct 2020
16 Oct 2020
Historique:
received:
30
09
2020
revised:
09
10
2020
accepted:
14
10
2020
entrez:
21
10
2020
pubmed:
22
10
2020
medline:
22
10
2020
Statut:
epublish
Résumé
Methylmercury (MeHg) is a well-known neurotoxicant that causes severe intoxication in humans. In Japan, it is referred to as Minamata disease, which involves two characteristic clinical forms: fetal type and adult type depending on the exposed age. In addition to MeHg burden level, individual susceptibility to MeHg plays a role in the manifestation of MeHg toxicity. Research progress has pointed out the importance of oxidative stress in the pathogenesis of MeHg toxicity. MeHg has a high affinity for selenohydryl groups, sulfhydryl groups, and selenides. It has been clarified that such affinity characteristics cause the impairment of antioxidant enzymes and proteins, resulting in the disruption of antioxidant systems. Furthermore, MeHg-induced intracellular selenium deficiency due to the greater affinity of MeHg for selenohydryl groups and selenides leads to failure in the recoding of a UGA codon for selenocysteine and results in the degradation of antioxidant selenoenzyme mRNA by nonsense-mediated mRNA decay. The defect of antioxidant selenoenzyme replenishment exacerbates MeHg-mediated oxidative stress. On the other hand, it has also been revealed that MeHg can directly activate the antioxidant Keap1/Nrf2 signaling pathway. This review summarizes the incidence of MeHg-mediated oxidative stress from the viewpoint of the individual intracellular redox system interactions and the MeHg-mediated aforementioned intracellular events. In addition, the mechanisms of cellular stress pathways and neuronal cell death triggered by MeHg-mediated oxidative stress and direct interactions of MeHg with reactive residues of proteins are mentioned.
Identifiants
pubmed: 33081221
pii: antiox9101004
doi: 10.3390/antiox9101004
pmc: PMC7602710
pii:
doi:
Types de publication
Journal Article
Review
Langues
eng
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