Role of Calcium and Mitochondria in MeHg-Mediated Cytotoxicity

• Published in: BioMed research international Vol. 2012; no. 2012; pp. 1 - 15
• Main Authors: Vargas Barbosa, Nilda, Puntel, Robson, Seeger, Rodrigo L., Roos, Daniel
• Format: Journal Article
• Language: English
• Published: Cairo, Egypt Hindawi Puplishing Corporation 01.01.2012; Hindawi Publishing Corporation; Hindawi Limited
• Subjects: Animals; Antioxidants; Antioxidants - pharmacology; Brain; Calcium; Calcium - metabolism; Cell Death - drug effects; Critical phenomena; Food chains; Homeostasis - drug effects; Humans; Methylmercury Compounds - chemistry; Methylmercury Compounds - toxicity; Mitochondria; Mitochondria - drug effects; Mitochondria - metabolism; Molecular weight; Neurotoxicity; Proteins; Review; Rodents; Studies
• ISSN: 1110-7243; 2314-6133; 1110-7251; 2314-6141
• DOI: 10.1155/2012/248764

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.