Protective effect of melatonin on beta-cell damage in streptozotocin-induced diabetes in rats


Yavuz O., Cam M., Bukan N., Guven A., Silan F.

ACTA HISTOCHEMICA, vol.105, no.3, pp.261-266, 2003 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 105 Issue: 3
  • Publication Date: 2003
  • Doi Number: 10.1078/0065-1281-00711
  • Journal Name: ACTA HISTOCHEMICA
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.261-266
  • Keywords: melatonin, diabetes mellitus, streptozotocin, oxidative stress, anti-insulin antibody, OXIDATIVE STRESS, LIPID-PEROXIDATION, GLUTATHIONE-PEROXIDASE, ANTIOXIDANT STATUS, PANCREATIC-ISLETS, IN-VITRO, MELLITUS, OXYGEN, TOXICITY, RADICALS
  • Gazi University Affiliated: Yes

Abstract

The aim of the present study was the evaluation of possible protective effects of melatonin against beta-cell damage in streptozotocin-induced diabetes in rats. Malondialdehyde levels and glutathione peroxidase activity were measured in pancreatic homogenates. Pancreatic beta-cells were examined by immunohistochemical methods. Streptozotocin was injected intraperitoneally at a single dose of 60 mg/kg for induction of diabetes. Melatonin (200 mug/kg/day, ip) was injected for 3 days prior to administration of streptozotocin; these injections were continued until the end of the study (4 weeks). Streptozotocin induced a significant increase in malondialdehyde levels (p < 0.01) and a significant decrease in glutathione peroxidase activity (p < 0.05) in pancreatic tissue. Degeneration of islet cells and weak immunohistochemical staining of insulin was observed in diabetic rats. Treatment of diabetic rats with melatonin markedly reduced malondialdehyde production (p < 0.05) and increased glutathione peroxidase activity (p < 0.01) without affecting hyperglycemia. Increased staining of insulin and preservation of islet cells were apparent in the melatonin-treated diabetic rats. These data suggest that melatonin treatment has a therapeutic effect in diabetes by reduction of oxidative stress and preservation of pancreatic beta-cell integrity.