Can trifluoperazine protect mitochondria against reactive oxygen species-induced damage?

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+.

Keywords

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