Imidaprilat suppresses nonylphenol and 1-methyl-4-phenylpyridinium ion (MPP+)-induced hydroxyl radical generation in rat striatum.

The present study examined the antioxidant effects of angiotensin-converting enzyme inhibitor (ACE), imidaprilat, on para-nonylphenol and 1-methyl-4-phenylpyridinium ion (MPP+)-induced hydroxyl radical (*OH) formation and dopamine (DA) efflux in extracellular fluid of rat striatum, using a microdialysis technique. para-Nonylphenol clearly enhanced *OH formation and DA efflux induced by MPP+. When imidaprilat was infused in para-nonylphenol and MPP+-treated rats, DA efflux and *OH formation significantly decreased, as compared with that in the para-nonylphenol and MPP+-treated control. Imidaprilat was able to scavenge *OH and DA efflux induced by para-nonylphenol and MPP+. When iron(II) was administered to para-nonylphenol-pretreated animals, iron(II) clearly produced a dose-dependent increase in the levels of 2,3-dihydroxybenzoic acid (2,3-DHBA), as compared with MPP+-only-treated rats. A positive linear correlation was observed between iron(II) and 2,3-DHBA (R2=0.985) in the dialysate. However, in the presence of imidaprilat, a small increase in the levels of 2,3-DHBA products was observed. The results suggest that imidaprilat may protect against para-nonylphenol and MPP+-induced *OH formation via suppressing DA efflux in the rat striatum.