Toxics 2018, 6(3), 47; https://doi.org/10.3390/toxics6030047
Oxidative Stress in Methylmercury-Induced Cell Toxicity
1
Department of Molecular Pharmacology, Albert Einstein College of Medicine, Bronx, NY 10461, USA
2
Laboratory of Toxicology, Medical School, University of Crete, 71003 Heraklion, Greece
3
Department of Medical Elementology, Peoples’ Friendship University of Russia (RUDN University), Moscow 150000, Russia
4
Laboratory of Biotechnology and Applied Bioelementology, Yaroslavl State University, Yaroslavl 150014, Russia
5
All-Russian Research Institute of Medicinal and Aromatic Plants (VILAR), Moscow 150000, Russia
6
Department of Biochemistry, Federal University of Santa Catarina, Florianopolis 88040-900, Santa Catarina, Brazil
7
Department of Biochemistry, Federal University of Santa Maria, Santa Maria 97105-900, Rio Grande do Sul, Brazil
*
Authors to whom correspondence should be addressed.
Received: 18 July 2018 / Revised: 3 August 2018 / Accepted: 7 August 2018 / Published: 9 August 2018
(This article belongs to the Special Issue Mercury and Methylmercury Toxicology and Risk Assessment)
Abstract
Methylmercury (MeHg) is a hazardous environmental pollutant, which elicits significant toxicity in humans. The accumulation of MeHg through the daily consumption of large predatory fish poses potential health risks, and the central nervous system (CNS) is the primary target of toxicity. Despite well-described neurobehavioral effects (i.e., motor impairment), the mechanisms of MeHg-induced toxicity are not completely understood. However, several lines of evidence point out the oxidative stress as an important molecular mechanism in MeHg-induced intoxication. Indeed, MeHg is a soft electrophile that preferentially interacts with nucleophilic groups (mainly thiols and selenols) from proteins and low-molecular-weight molecules. Such interaction contributes to the occurrence of oxidative stress, which can produce damage by several interacting mechanisms, impairing the function of various molecules (i.e., proteins, lipids, and nucleic acids), potentially resulting in modulation of different cellular signal transduction pathways. This review summarizes the general aspects regarding the interaction between MeHg with regulators of the antioxidant response system that are rich in thiol and selenol groups such as glutathione (GSH), and the selenoenzymes thioredoxin reductase (TrxR) and glutathione peroxidase (Gpx). A particular attention is directed towards the role of the PI3K/Akt signaling pathway and the nuclear transcription factor NF-E2-related factor 2 (Nrf2) in MeHg-induced redox imbalance. View Full-TextKeywords:
methylmercury; oxidative stress; molecular mechanisms
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Antunes dos Santos, A.; Ferrer, B.; Marques Gonçalves, F.; Tsatsakis, A.M.; Renieri, E.A.; Skalny, A.V.; Farina, M.; Rocha, J.B.T.; Aschner, M. Oxidative Stress in Methylmercury-Induced Cell Toxicity. Toxics 2018, 6, 47.
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