In vivo effect of vitamin C with cobalt on oxidative stress in experimental diabetic rat kidney

O Yildirim1, Z Büyükbingöl

  • 1Faculty of Science, Department of Biology, Ankara University, Tandogan, Ankara, Turkey. ozlemesn@hotmail.com

Diabetes, Nutrition & Metabolism
|February 11, 2004
PubMed

Insights

Diabetic rats showed increased kidney oxidative stress markers and decreased vitamin C levels. Treatment with vitamin C and cobalt partially restored some markers but did not fully reverse kidney damage.

Area of Science:

  • Biochemistry
  • Toxicology
  • Endocrinology

Background:

  • Diabetes mellitus is associated with increased oxidative stress.
  • Kidney damage in diabetes can be exacerbated by oxidative stress.
  • Antioxidants like vitamin C may play a role in mitigating diabetic complications.

Purpose of the Study:

  • To investigate the effects of vitamin C and cobalt on kidney oxidative stress markers in diabetic rats.
  • To evaluate the therapeutic potential of vitamin C and cobalt in managing diabetic nephropathy.

Main Methods:

  • Diabetes was induced in rats using streptozotocin.
  • Treated rats received vitamin C (1 g/l) with cobalt chloride (0.5 mM) in drinking water for 6 weeks.
  • Kidney enzyme activities (superoxide dismutase, glutathione peroxidase, catalase), vitamin C levels, and lipid peroxidation were measured.

Main Results:

  • Diabetic rats exhibited significantly increased kidney superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) activities, and lipid peroxidation.
  • Vitamin C levels were significantly decreased in diabetic rats.
  • Vitamin C with cobalt treatment partially restored SOD and CAT activities, and vitamin C levels, but did not affect GSH-Px activity.

Conclusions:

  • Vitamin C with cobalt treatment effectively normalized hyperglycemia in diabetic rats at 6 weeks.
  • The treatment partially restored altered endogenous defense systems in the diabetic rat kidney but could not completely reverse the damage.
  • Further research is needed to fully understand the mechanisms and optimize therapeutic strategies for diabetic nephropathy.

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