Fe(III) shifts the mitochondria permeability transition-eliciting capacity of mangiferin to protection of organelle / s. t
J Pharmacol Exp Ther
; 320(2)Oct. 2006. graf, tab
Artigo
em Inglês
| CUMED
| ID: cum-40044
Biblioteca responsável:
CU1.1
ABSTRACT
Mangiferin acts as a strong antioxidant on mitochondria. However, when in the presence of Ca(2+), mangiferin elicits mitochondrial permeability transition (MPT), as evidenced by cyclosporin A-sensitive mitochondrial swelling. We now provide evidence, by means of electrochemical and UV-visible spectroscopical analysis, that Fe(III) coordinates with mangiferin. The resulting mangiferin-Fe(III) complex does not elicit MPT and prevents MPT by scavenging reactive oxygen species. Indeed, the complex protects mitochondrial membrane protein thiols and glutathione from oxidation. Fe(III) also significantly increases the ability of mangiferin to scavenge the 2,2-diphenyl-1-picrylhydrazyl radical, as well as to display antioxidant activity toward antimycin A-induced H(2)O(2) production and t-butyl hydroperoxide-promoted membrane lipid peroxidation in mitochondria. We postulate that coordination with Fe(III) constitutes a potential protective mechanism toward the prooxidant action of mangiferin and other catechol-containing antioxidants regarding MPT induction. Potential therapeutic relevance of this finding for conditions of pathological iron overload is discussed(AU)
Texto completo:
Disponível
Coleções:
Bases de dados nacionais
/
Cuba
Base de dados:
CUMED
Assunto principal:
Organelas
/
Xantonas
/
Ferro
/
Mitocôndrias
Limite:
Animais
Idioma:
Inglês
Revista:
J Pharmacol Exp Ther
Ano de publicação:
2006
Tipo de documento:
Artigo
Instituição/País de afiliação:
Universidad de La Habana/Cuba
/
Universidad de Zulia/Brazil