ISSN:
1573-6903
Keywords:
Free radicals
;
kainic acid
;
cortical neuron
;
a-phenyl-N-tert-butyl-nitrone
;
excitotoxicity
;
xanthine oxidase
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Abstract In our previous experiments, evidence of free radical formation has been demonstrated in gerbil brain after kainic acid (KA) administration. In the present study, the mechanisms involved in KA-induced free radical formation and subsequent cell degeneration were investigated using high density cortical neuron cultures. A free radical trapping agent,a-phenyl-N-tert-butyl-nitrone (PBN), as well as the combined action of superoxide dismutase and catalase attenuated KA neurotoxic effect. Calpain-induced xanthine oxidase (XO) activation may play an important role in KA excitotoxicity since calpain inhibitor I as well as allopurinol, a selective XO inhibitor, significantly protected the cortical neurons from KA-induced cell death. However, XO activation may not be the only source producing free radicals, other free radical generating systems such as nitric oxide synphase may also play a role in KA insult.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00969006
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