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REVIEW ARTICLE
Year : 2008  |  Volume : 128  |  Issue : 4  |  Page : 373-382

Methylmercury neurotoxicity & antioxidant defenses


1 Lab. Neuroquímica Molecular e Celular, Dep. Fisiologia, Instituto de Ciências Biológicas, Universidade Federal do Pará, Belém, PA, Brazil
2 Lab. Farmacologia Molecular, Instituto de Ciências Biológicas, Universidade Federal do Pará, Belém, PA, Brazil
3 Núcleo de Medicina Tropical, Universidade Federal do Pará, Belém, PA, Brazil
4 Núcleo de Medicina Tropical, Universidade Federal do Pará, Belém, PA, Brazil; Lab. Neurofisiologia, Instituto de Ciências Biológicas, Universidade Federal do Pará, Belém, PA, Brazil
5 Lab. Neuroquímica Molecular e Celular, Dep. Fisiologia, Instituto de Ciências Biológicas, Universidade Federal do Pará, Belém, PA, Brazil; Lab. Neuroendocrinologia Instituto de Ciências Biológicas, Universidade Federal do Pará, Belém, PA, Brazil

Correspondence Address:
José Luiz M. do Nascimento
Lab. Neuroquímica Molecular e Celular, Dep. Fisiologia, Instituto de Ciências Biológicas, Universidade Federal do Pará, Belém, PA, Brazil

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Source of Support: None, Conflict of Interest: None


PMID: 19106435

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Neurotoxicity induced by methylmercury (MeHg) increases the formation of reactive radicals and accelerates free radical reactions. This review summarizes recent findings in the MeHg-induced formation of free radicals and the role of oxidative stress in its neurotoxicity. Oxidative stress on CNS can produce damage by several interacting mechanisms, including mitochondrial damage with increase in intracellular free Ca(2+), activation and inhibition of enzymes, release of excitatory amino acids, metallothioneins expression, and microtubule disassembly. The nature of antioxidants is discussed and it is suggested that antioxidant enzymes and others antioxidants molecules may protect the central nervous system against neurotoxicity caused by MeHg.


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