DNA protective and antioxidative effects of melatonin in streptozotocin-induced diabetic rats

Abstract

Diabetes mellitus is a chronic disease characterized by elevated blood sugar levels. In diabetic patients, oxidative stress induced by the presence of excessive free radicals is closely associated with chronic inflammation, leading to potential tissue damage. Melatonin (MEL) is a compound synthesized by the pineal gland and a scavenger of free radicals. The aim of this study was to research the effects of MEL on oxidative stress and its DNA protective effects in streptozotocin-induced diabetic rats. In total, 32 rats were equally divided into four experimental groups: control, melatonin, diabetic, and diabetic + melatonin. A single dose of streptozotocin (60 mg/kg) was given by intraperitoneal route to induce experimental diabetes. MEL (10 mg/kg daily) was administrated to rats by intraperitoneal route for 6 weeks. Oxidative stress parameters were evaluated in rat liver, kidney, brain, and pancreas tissues. Body weight, plasma glucose, and HbA 1c levels were studied. DNA damage was analyzed by comet assay in lymphocytes, while % tail DNA and mean tail moment parameters were evaluated. The study results indicate that the intraperitoneal administration of 10 mg/kg MEL over 6 weeks may cause amelioration in oxidative stress parameters against diabetes, leading to beneficial effects based on % tail DNA and mean tail moment parameters in rat lymphocytes.

Impact of Betanin on Diabetes Induced Experimentally by Streptozotocin and Associated Histopathological Changes in Albino Adult Rats

“…The current study's findings demonstrated that STZ injection caused the blood glucose level in the diabetic group to significantly increase as contrasted with control group, while glycated haemoglobin levels substantially decreased. These findings concur with those of Sekkin et al (15) 's research who reported a single STZ injection results in the onset of diabetes mellitus., which is identified by raised blood sugar, glycated haemoglobin, and drop serum insulin levels. This happened because STZ generated an inflammatory response that resulted in macrophage and later lymphocyte infiltration, damaged the islets cells, destroyed the cells within twenty-four hours, and triggered an immune response.…”

Antihyperglycemic, Antioxidant and Antiapoptotic Effect of Rhizophora Mucronata and Avicennia Marina in Streptozotocin-induced Diabetic Rats

“…The over generation of ROS, LPO, and diminished tissue concentrations of SOD, CAT, and GSH were reported in both clinical and experimental models of diabetes ( 23 ). Similar findings were reported in different tissues, such as diabetic rat’s liver, kidney, and pancreas ( 24 ), heart ( 25 ), as well as blood ( 26 ).…”

“…It is a direct scavenger of free radicals as well as a co-substrate for peroxide detoxification by GPX. Increased GSH level might have been sustained to counteract fast-generating oxygen radicals and concomitantly protect tissue cells from ROS and peroxides ( 24 ).…”

Efficacy of melatonin in restoring the antioxidant status in the lens of diabetic rats induced by streptozotocin

“…In the present study, we observed that induction of diabetes decreased the plasma GSH concentration in the rats and administration of melatonin increased the GSH levels significantly near to healthy control rats. Sekkin et al demonstrated that induction of diabetes caused depletion in GSH in the pancreas tissue and treatment with melatonin for 6 weeks elevated the GSH levels significantly [34]. Klepac et al also, reported that melatonin (20 mg/kg, ip) increased the plasma GSH concentration in diabetic rats by 9% after a single injection [7].…”