Open AccessNitric oxide synthase inhibitors prevents quinolinic acid-induced neurotoxicity: the role of nitric oxide and glucose-6-phosphate dehydrogenase in cell death
Author(s) -
D Ivana Maksimovic,
D Marina Jovanovic,
J Miodrag Colic,
Dejan Mićić,
R. Mihajlović,
Mirjana Selaković
Publication year - 2002
Publication title -
jugoslovenska medicinska biohemija
Language(s) - English
Resource type - Journals
eISSN - 1452-8193
pISSN - 0354-3447
DOI - 10.2298/jmh0203269m
Subject(s) - quinolinic acid , nitric oxide synthase , nitric oxide , chemistry , neurotoxicity , biochemistry , pharmacology , forebrain , neurotoxin , nitrite , endocrinology , toxicity , biology , central nervous system , amino acid , tryptophan , organic chemistry , nitrate
In the present study we employed Nw-nitro-L-arginine methyl ester, non-specific potent nitric oxide synthase inhibitor and a selective inhibitor of neuronal nitric oxide synthase, 7-nitroindazole, reportedly to investigate the possible involvement of nitric oxide in quinolinic acid-induced striatal toxicity in the rat. Quinolinic acid was administered unilaterally into striatum of adult Wistar rats in the single dose of 150 nmol/L. The other two group of animals were pretreated with Nw-nitro-L-arginine methyl ester and 7-nitroindazole respectively. Control groups of animals were treated with 0,154 mmol/L saline solution likewise. Nitrite levels was decreased in the ipsi- and contralateral striatum and forebrain cortex in the group treated with nitric oxide synthase inhibitors and neurotoxin compared to quinolinic acid-treated animals. In the same structures, activity of glucose-6-phosphate dehydrogenase was also decreased, compared to quinolinic acid-treated animals. These results indicate that application of the nitric oxide synthase inhibitors, supressed nitrite accumulation and glucose-6-phosphate dehydrogenase activity and attenuated quinolinic acid-induced neuronal damage in the striatum and forebrain cortex.