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Journal of Biomedicine and Biotechnology
Volume 2012 (2012), Article ID 248764, 15 pages
Review Article

Role of Calcium and Mitochondria in MeHg-Mediated Cytotoxicity

1Departamento de Química, CCNE, Programa de Pós-Graduação em Bioquímica Toxicológica, Universidade Federal de Santa Maria, 97105.900 Santa Maria, RS, Brazil
2Universidade Federal do Pampa-Campus Uruguaiana, BR-472 Km 7, 97500-970 Uruguaiana, RS, Brazil

Received 6 April 2012; Revised 12 June 2012; Accepted 14 June 2012

Academic Editor: Marcelo Farina

Copyright © 2012 Daniel Roos et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Methylmercury (MeHg) mediated cytotoxicity is associated with loss of intracellular calcium (Ca2+) homeostasis. The imbalance in Ca2+ physiology is believed to be associated with dysregulation of Ca2+ intracellular stores and/or increased permeability of the biomembranes to this ion. In this paper we summarize the contribution of glutamate dyshomeostasis in intracellular Ca2+ overload and highlight the mitochondrial dysfunctions induced by MeHg via Ca2+ overload. Mitochondrial disturbances elicited by Ca2+ may involve several molecular events (i.e., alterations in the activity of the mitochondrial electron transport chain complexes, mitochondrial proton gradient dissipation, mitochondrial permeability transition pore (MPTP) opening, thiol depletion, failure of energy metabolism, reactive oxygen species overproduction) that could culminate in cell death. Here we will focus on the role of oxidative stress in these phenomena. Additionally, possible antioxidant therapies that could be effective in the treatment of MeHg intoxication are briefly discussed.