Can trifluoperazine protect mitochondria against reactive oxygen species-induced damage?
Nenhuma Miniatura disponível
Data
1996-12-01
Autores
Orientador
Coorientador
Pós-graduação
Curso de graduação
Título da Revista
ISSN da Revista
Título de Volume
Editor
Tipo
Artigo
Direito de acesso
Acesso restrito
Resumo
Trifluoperazine (TFP) (35 μM) prevents mitochondrial transmembrane potential (ΔΨ) collapse and swelling induced by 10 μM Ca2+ plus oxyradicals generated from δ-aminolevulinic acid autoxidation. In contrast with EGTA, TFP cannot restore the totally collapsed ΔΨ. So, TFP might not remove Ca2+ from its 'harmful site', but could impair the ROS-driven cross-linking between membrane -SH proteins. Our data are correlated with the protective uses of TFP against oxidative processes promoted by oxyradicals plus Ca2+.
Descrição
Palavras-chave
Ca2+, Mitochondria, Oxidative stress, Reactive oxygen species, Trifluoperazine, reactive oxygen metabolite, trifluoperazine, animal tissue, liver disease, liver mitochondrion, membrane potential, mitochondrial membrane, mitochondrion swelling, nonhuman, oxidative stress, rat, Aminolevulinic Acid, Animals, Calcium, Membrane Potentials, Mitochondria, Liver, Oxidation-Reduction, Permeability, Rats, Rats, Wistar, Reactive Oxygen Species
Idioma
Inglês
Como citar
European Journal of Drug Metabolism and Pharmacokinetics, v. 21, n. 4, p. 281-284, 1996.
