Angiotensin II receptor blockage prevents diabetes-induced oxidative damage in rat heart


ÖZDEMİR S., Tandogan B., Ulusu N., TURAN B.

Folia Biologica, vol.55, no.1, pp.11-16, 2009 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 55 Issue: 1
  • Publication Date: 2009
  • Journal Name: Folia Biologica
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.11-16
  • Keywords: oxidative stress, renin-angiotensin system, type 1 diabetes, antioxidant enzymes, heart, SUPEROXIDE-PRODUCTION, ANTIOXIDANT ENZYMES, LIPID-PEROXIDATION, STRESS, AORTA, ACTIVATION, OXIDASE, SYSTEM, TISSUE
  • Lokman Hekim University Affiliated: No

Abstract

Current findings suggest a role for the angiotensin II (Ang II) signalling pathway in generation of reactive oxygen species and diabetes-induced cardiac complications. In this study we aimed to investigate the effect of angiotensin II type 1 (AT1) receptor blockage on some antioxidant enzymes such as glucose-6-phosphate dehydrogenase (G6PD), 6-phoshogluconate dehydrogenase (6PGD), glutathione reductase (GR), glutathione-S-transferase (GST), glutathione peroxidase (GSH-Px), and catalase (CAT) in the heart of streptozotocin (STZ)-induced diabetic rats. The effect of AT1 receptor blocker, candesartan-cilexetil (5 mg/ kg/day for 4 weeks) was studied. Diabetes caused hyperglycaemia (4-fold of control) with significant increases in G6PD, 6PGD, GR, GSH-PX, CAT and no effect on GST in heart tissues as compared to normal control rats. Treatment of STZ-induced diabetic rats with candesartan-cilexetil had significant beneficial effects on these parameters without any side effect on control rats. These results suggest that Ang II can take part in induction of oxidative stress in diabetic rat heart and that blockage of its activity by AT1 receptor blocker is potentially protective against diabetes-induced cellular damage.