Nitric oxide synthase inhibition by L-NAME in streptozotocin induced diabetic rats: impacts on oxidative stress

Tohoku J Exp Med. 2003 Apr;199(4):205-10. doi: 10.1620/tjem.199.205.

Abstract

The effects of nitric oxide synthase (NOS) inhibition by Nw-nitro-L-arginine methyl ester (L-NAME) administration on oxidative stress parameters were investigated in streptozotocin (STZ) induced diabetic rats. Lipid peroxidation as reflected by thiobarbituric acid reactive substances (TBARS) was insignificantly higher in diabetic rats. Plasma NO2+NO3 values (p < 0.05) and erythrocyte CuZn superoxide dismutase (CuZn SOD) and glutathione peroxidase (GSH Px) activities were significantly higher (p < 0.01, p < 0.001, respectively) in diabetic rats. L-NAME administration to diabetic rats caused significantly lower CuZn SOD and GSH Px activities (p < 0.01) and NO2+NO3 values (p < 0.001), whereas a significantly higher GSH level (p < 0.01). TBARS/GSH ratio was significantly higher in diabetic rats than controls (p < 0.05) and significantly lower in L-NAME administered diabetic rats than diabetic rats (p < 0.05). This experimental study highlightens the importance of NOS inhibition by L-NAME in the attenuation of oxidative stress in STZ diabetic rats.

MeSH terms

  • Animals
  • Diabetes Mellitus, Experimental / metabolism*
  • Erythrocytes / metabolism
  • Glutathione / blood
  • Glutathione Peroxidase / metabolism
  • Lipid Peroxidation / drug effects
  • Male
  • NG-Nitroarginine Methyl Ester / pharmacology*
  • Nitric Oxide / blood
  • Nitric Oxide Synthase / antagonists & inhibitors*
  • Oxidative Stress / drug effects*
  • Rats
  • Rats, Wistar
  • Superoxide Dismutase / metabolism
  • Thiobarbituric Acid Reactive Substances / metabolism

Substances

  • Thiobarbituric Acid Reactive Substances
  • Nitric Oxide
  • Glutathione Peroxidase
  • Nitric Oxide Synthase
  • Superoxide Dismutase
  • Glutathione
  • NG-Nitroarginine Methyl Ester