Renal cortical expression of mRNAs for antioxidant enzymes in normal and diabetic rats

Alluru Reddi, Jaya S. Bollineni

Research output: Contribution to journalArticle

40 Citations (Scopus)

Abstract

Increased oxidative stress has been implicated in the development of vascular complications of diabetes. In this study, we examined the hypothesis whether chronic hyperglycemia induces oxidative stress by lowering renal expression and activity of antioxidant enzymes and a decrease in glutathione, an antioxidant, in streptozotocin diabetic rats. The results show that the expression of mRNAs for Cu/Zn superoxide dismutase and glutathione peroxidase was significantly increased and that of catalase was decreased in diabetic rats. However, the superoxide dismutase activity was significantly lower in diabetic than normal glomeruli, whereas the activities of the other two enzymes correlated with their mRNA expression. Total glutathione content was significantly decreased in diabetic compared to normal glomeruli. The data suggest that hyperglycemia induces oxidative stress by overexpressing rather than lowering certain antioxidant enzyme mRNAs in the kidney of diabetic rats. Enhanced nonenzymatic glycation of enzyme protein seems to be the cause for the observed decrease in glomerular superoxide dismutase activity.

Original languageEnglish (US)
Pages (from-to)598-601
Number of pages4
JournalBiochemical and Biophysical Research Communications
Volume235
Issue number3
DOIs
StatePublished - Jun 27 1997

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Oxidative stress
Rats
Antioxidants
Kidney
Messenger RNA
Oxidative Stress
Enzymes
Hyperglycemia
Superoxide Dismutase
Glutathione
Diabetes Complications
Streptozocin
Medical problems
Glutathione Peroxidase
Catalase
Blood Vessels
Proteins

All Science Journal Classification (ASJC) codes

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

Cite this

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Renal cortical expression of mRNAs for antioxidant enzymes in normal and diabetic rats. / Reddi, Alluru; Bollineni, Jaya S.

In: Biochemical and Biophysical Research Communications, Vol. 235, No. 3, 27.06.1997, p. 598-601.

Research output: Contribution to journalArticle

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