Yavuz, ÖzlemCam, MeryemBukan, NeslihanGüven, AyselSılan, Fatma2021-06-232021-06-2320030065-1281https://doi.org/10.1078/0065-1281-00711https://hdl.handle.net/20.500.12491/5511The 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.eninfo:eu-repo/semantics/closedAccessMelatoninDiabetes MellitusStreptozotocinOxidative StressAnti-insulin AntibodyArticle10.1078/0065-1281-007111053261266136776202-s2.0-0041877508Q3WOS:000185139500008Q4