Citation

Antunes Dos Santos A, Appel Hort M, Culbreth M, López-Granero C, Farina M, Rocha JB, Aschner M. J. Trace Elem. Med. Biol. 2016; 38: 99-107.

Affiliation

Department of Molecular Pharmacology, Albert Einstein College of Medicine, Bronx, NY, USA. Electronic address: Michael.aschner@einstein.yu.edu.

Copyright

(Copyright © 2016, Elsevier Publishing)

DOI

10.1016/j.jtemb.2016.03.001

PMID

26987277

Abstract

Methylmercury (MeHg) is a potent environmental pollutant, which elicits significant toxicity in humans. The central nervous system (CNS) is the primary target of toxicity, and is particularly vulnerable during development. Maternal exposure to MeHg via consumption of fish and seafood can have irreversible effects on the neurobehavioral development of children, even in the absence of symptoms in the mother. It is well documented that developmental MeHg exposure may lead to neurological alterations, including cognitive and motor dysfunction. The neurotoxic effects of MeHg on the developing brain have been extensively studied. The mechanism of toxicity, however, is not fully understood. No single process can explain the multitude of effects observed in MeHg-induced neurotoxicity. This review summarizes the most current knowledge on the effects of MeHg during nervous system development considering both, in vitro and in vivo experimental models. Considerable attention was directed towards the role of glutamate and calcium dyshomeostasis, mitochondrial dysfunction, as well as the effects of MeHg on cytoskeletal components/regulators.

Copyright © 2016 Elsevier GmbH. All rights reserved.

Language: en