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Abstract
Mercury (Hg) toxicity is governed by cellular thiol compounds and its capacity to generate reactive oxygen radicals and oxidative stress. Selenium (Se) plays a key role in the prevention of the toxic effects of Hg by modulating the activity of several Se-dependent enzymes, including glutathione peroxidase (GSH-Px). In addition, dietary Se can reduce Hg toxicity by directly interacting with either Hg(II) or methylmercury (MeHg) to form inert products, such as HgSe complexes. Although experimental and environmental data have indicated a protective role for selenium against Hg toxicity, human data are more limited and somewhat controversial. In the Amazon Region of Brazil, Hg pollution is rampant as a result of gold (Au) mining and other anthropogenic factors, leading to the pervasive release of large quantities of metallic Hg0 into the environment. Exposure to Hg in this region is associated with direct occupational exposure in the gold mining industry, as well as consumption by inhabitants of riverside communities of a diet rich in MeHg-contaminated fish. Human exposure to MeHg in the Amazon through the diet has been monitored by measuring Hg and MeHg in hair samples. In this paper, we review the environmental contamination of Hg in the Amazon and detail human exposures in populations of this region. We conclude with a brief synopsis on Se levels in the Amazon population and provide a brief review of data available on the interaction between Hg and Se in this region. Overall, the literature supports the notion that low environmental Se is linked to susceptibility to Hg toxicity and that Se levels could be used as a bioindicator to monitor the health of Hg-exposed subjects. However, in light of the limited human data on this subject, further epidemiological studies are needed to clarify how changes in Se levels modify the toxicity of environmental Hg.
ACKNOWLEDGEMENTS
This research was supported by grants from Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) – Programa de Núcleos de Excelência (PRONEX) / Fundação de Amparo à Pesquisa do Estado do Pará (FAPESPA) #2268, Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) #486351/ 2006-8, Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) #620037/2008-3, and Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) – Proequipamentos (PROEQUIP) #1649/2007. LCLS and JBTR are CNPq research fellows. Supported by the Financiadora de Estudos e Pesquisas (FINEP) research grant “Rede Instituto Brasileiro de Neurociência (IBN-Net)” #01.06.0842-00. MA was supported in part by a grant from the National Institute of Environmental Health Sciences (NIEHS 07331).