TY - JOUR
T1 - Protective effect of captopril and enaraprilat, angiotensin-converting enzyme inhibitors, on para-nonylphenol-induced {radical dot}OH generation and dopamine efflux in rat striatum
AU - Obata, Toshio
AU - Takahashi, Shigehiro
AU - Kashiwagi, Yoshitomo
AU - Kubota, Shunichiro
N1 - Funding Information:
This study was supported by Health Science Research Grants for Research on Environmental Health from the Ministry of Health and Welfare of Japan, and a grant under the Ministry of Education, Science, Sports, and Culture, Japan.
PY - 2008/9/4
Y1 - 2008/9/4
N2 - 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.
AB - 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.
KW - 1-Methyl-4-phenylpyridinium ion (MPP)
KW - Angiotensin-converting enzyme inhibitor
KW - Dopamine
KW - Hydroxyl radical
KW - Striatum
KW - para-Nonylphenol
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U2 - 10.1016/j.tox.2008.06.005
DO - 10.1016/j.tox.2008.06.005
M3 - Article
C2 - 18611425
AN - SCOPUS:49849104484
VL - 250
SP - 96
EP - 99
JO - Toxicology
JF - Toxicology
SN - 0300-483X
IS - 2-3
ER -