Protective effect of captopril and enaraprilat, angiotensin-converting enzyme inhibitors, on para-nonylphenol-induced {radical dot}OH generation and dopamine efflux in rat striatum

We recently reported that para-nonylphenol, an environmental chemical, induced hydroxyl radical ({radical dot}OH) formation in rat striatum. In this study we examined the antioxidant effects of angiotensin-converting enzyme inhibitors (captopril or enalaprilat) on para-nonylphenol (nonylphenol) and 1-methyl-4-phenylpyridinium ion (MPP⁺)-induced hydroxyl radical ({radical dot}OH) formation and dopamine (DA) efflux in extracellular fluid of rat striatum, using a microdialysis technique. para-Nonylphenol clearly enhanced {radical dot}OH formation and DA efflux induced by MPP⁺. When captopril or enalaprilat was infused in nonylphenol and MPP⁺-treated rats, DA efflux and {radical dot}OH formation significantly decreased, as compared with that in the nonylphenol and MPP⁺-treated control. We compared the ability of non-SH-containing enalaprilat with a SH-containing captopril to scavenge {radical dot}OH and DA efflux. Both inhibitors were able to scavenge {radical dot}OH and DA efflux induced by para-nonylphenol and MPP⁺. The results suggest that angiotensin-converting enzyme inhibitors may protect against nonylphenol and MPP⁺-induced {radical dot}OH formation via suppressing DA efflux in the rat striatum.