Oxidative mechanisms involved in kainate-induced cytotoxicity in cortical neurons

Neurochem Res. 1994 Dec;19(12):1557-64. doi: 10.1007/BF00969006.


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, alpha-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 synthase may also play a role in KA insult.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Allopurinol / pharmacology
  • Animals
  • Calpain / pharmacology
  • Catalase / pharmacology
  • Cell Death / drug effects*
  • Cells, Cultured
  • Cerebral Cortex / cytology*
  • Cyclic N-Oxides
  • Enzyme Activation / drug effects
  • Female
  • Free Radical Scavengers
  • Free Radicals
  • Glycoproteins / pharmacology
  • Kainic Acid / pharmacology*
  • Nitrogen Oxides / pharmacology
  • Oxidation-Reduction
  • Pregnancy
  • Rats
  • Rats, Sprague-Dawley
  • Superoxide Dismutase / pharmacology
  • Xanthine Oxidase / metabolism


  • Cyclic N-Oxides
  • Free Radical Scavengers
  • Free Radicals
  • Glycoproteins
  • Nitrogen Oxides
  • calpain inhibitors
  • phenyl-N-tert-butylnitrone
  • Allopurinol
  • Catalase
  • Superoxide Dismutase
  • Xanthine Oxidase
  • Calpain
  • Kainic Acid