Lipid peroxidation and antioxidant status in experimental diabetes

Clin Chim Acta. 1999 Jun 15;284(1):31-43. doi: 10.1016/s0009-8981(99)00046-7.


Oxidative stress is currently suggested as a mechanism underlying diabetes. The present study was designed to evaluate the oxidative stress related parameters in streptozotocin-induced diabetes in rats using different complementary approaches: susceptibility to in vitro oxidation (lipid peroxidation induction in liver homogenate, red blood cells hemolysis), blood antioxidant status (total antioxidant capacity by two approaches), and plasma isoprostane measurement, a new marker of lipid peroxidation in vivo. We have shown that induced liver thiobarbituric acid reactive substances increased after 4 weeks of diabetes, in spite of increased liver vitamin E content. Red blood cells hemolysis was significantly delayed after 4 weeks of diabetes. Plasma antioxidant capacity (AOC) tended to increase after 4 weeks of diabetes and was correlated with plasma vitamin E levels. Total antioxidant activity (TAA) significantly decreased after 1 week and a significant correlation was observed with plasma albumin levels. Plasma isoprostane (8-epiprostaglandinF2alpha) concentrations were not modified significantly 1 week or 4 weeks after the induction of diabetes. Levels of vitamin E in the diet and changes in its distribution among the body seems to play an important role in the development of oxidative stress during diabetes and its consequences.

MeSH terms

  • Animals
  • Antioxidants / metabolism*
  • Arachidonic Acid / blood
  • Diabetes Mellitus, Experimental / blood
  • Diabetes Mellitus, Experimental / metabolism*
  • Dinoprost / analogs & derivatives
  • Dinoprost / blood
  • Hemolysis
  • Lipid Peroxidation*
  • Liver / metabolism
  • Male
  • Oxidative Stress
  • Rats
  • Rats, Wistar
  • Streptozocin
  • Triglycerides / metabolism


  • Antioxidants
  • Triglycerides
  • 8-epi-prostaglandin F2alpha
  • Arachidonic Acid
  • Streptozocin
  • Dinoprost