Efeito de antioxidantes sobre os níveis de metalotioneínas em camundongos tratados com cloreto de mercúrio

Detalhes bibliográficos
Ano de defesa: 2006
Autor(a) principal: Brandão, Ricardo
Orientador(a): Não Informado pela instituição
Banca de defesa: Não Informado pela instituição
Tipo de documento: Dissertação
Tipo de acesso: Acesso aberto
Idioma: por
Instituição de defesa: Universidade Federal de Santa Maria
BR
Bioquímica
UFSM
Programa de Pós-Graduação em Ciências Biológicas: Bioquímica Toxicológica
Programa de Pós-Graduação: Não Informado pela instituição
Departamento: Não Informado pela instituição
País: Não Informado pela instituição
Palavras-chave em Português:
Link de acesso: http://repositorio.ufsm.br/handle/1/11142
Resumo: In this study, acute effects of mercury on mouse blood, kidneys and liver were evaluated. Mice received a single dose of mercuric chloride (HgCl2 - 4.6 mg/kg, subcutaneously) for three consecutive days. We investigated the possible beneficial effects of antioxidant therapy (N-acetylcysteine (NAC) and diphenyl diselenide (PhSe)2) comparing to sodium salt of 2,3-dimercapto-1-propanesulfonic acid (DMPS), an effective chelating agent on mercury exposure in mice. We also verified if metallothionein (MT) induction would be involved in a possible mechanism of protection against mercury poisoning and if different therapies would modify MT levels and other toxicological parameters. The results demonstrated that animals treated with mercuric chloride presented a reduction in the body weight gain and therapies did not were effective in reverting this damage. HgCl2 exposure inhibited δ-aminolevulinic dehydratase (δ-ALA-D) activity in liver and only DMPS treatment prevented the inhibitory effect. Animals treated with mercury presented an increase in renal NPSH and therapies did not modify these levels. Urea concentration was increased after mercury exposure. NAC plus (PhSe)2 was partially effective in protecting against this effect of mercury . DMPS and (PhSe)2 were effective in restoring the increment in urea concentration caused by mercury. Thiobarbituric acid-reactive substances (TBARS), ascorbic acid levels, aspartate (AST) and alanine (ALT) aminotransferases were not modified after mercury exposure. Moreover, mercury poisoning caused an increase in hepatic and renal MT levels and antioxidant therapies did not modify this parameter. Our data pointed out the lack of the therapeutic effect of antioxidants tested.