dc.contributorUniversidade Estadual Paulista (Unesp)
dc.contributorUniversidade de Brasília (UnB)
dc.date.accessioned2014-05-27T11:18:08Z
dc.date.available2014-05-27T11:18:08Z
dc.date.created2014-05-27T11:18:08Z
dc.date.issued1996-12-01
dc.identifierEuropean Journal of Drug Metabolism and Pharmacokinetics, v. 21, n. 4, p. 281-284, 1996.
dc.identifier0378-7966
dc.identifierhttp://hdl.handle.net/11449/64893
dc.identifier10.1007/BF03189728
dc.identifierWOS:A1996WM98400001
dc.identifier2-s2.0-0030498766
dc.description.abstractTrifluoperazine (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+.
dc.languageeng
dc.relationEuropean Journal of Drug Metabolism and Pharmacokinetics
dc.relation1.362
dc.relation0,338
dc.rightsAcesso restrito
dc.sourceScopus
dc.subjectCa2+
dc.subjectMitochondria
dc.subjectOxidative stress
dc.subjectReactive oxygen species
dc.subjectTrifluoperazine
dc.subjectreactive oxygen metabolite
dc.subjecttrifluoperazine
dc.subjectanimal tissue
dc.subjectliver disease
dc.subjectliver mitochondrion
dc.subjectmembrane potential
dc.subjectmitochondrial membrane
dc.subjectmitochondrion swelling
dc.subjectnonhuman
dc.subjectoxidative stress
dc.subjectrat
dc.subjectAminolevulinic Acid
dc.subjectAnimals
dc.subjectCalcium
dc.subjectMembrane Potentials
dc.subjectMitochondria, Liver
dc.subjectOxidation-Reduction
dc.subjectPermeability
dc.subjectRats
dc.subjectRats, Wistar
dc.subjectReactive Oxygen Species
dc.titleCan trifluoperazine protect mitochondria against reactive oxygen species-induced damage?
dc.typeArtículos de revistas


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