RESUMEN
BACKGROUND: An increase in oxidative stress has been suggested to play major roles in the complications of diabetes. The bulk of the experimental data favors enhanced free radicals in diabetes and antioxidant defense mechanisms may be reduced in diabetes. Melatonin, the major secretory product of the pineal gland has been shown to be a potent and specific hydroxyl radical scavenger. The purpose of our study was to determine the antioxidative effeet of melatonin in streptozotocin-induced diabetic rats. METHODS: Sprague-Dawley rats weighing 200-240 g were divided into 3 groups: normal controls(n-7), diabetic contmls(n-9), melatonin-treated diabetic animals(n-9). Diabetes was induced by intraperitoneal injection of streptozotoein(55 mg/kg body weight) and melatonin(6 mg/kg body weight) was orally administered for 20 days. At day 20 after streptozotocin administration, blood was collected for the assay of glucose, albumin and cholesterol. Erythrocyte membrane lipid peroxidation was determined by malonyldialdehyde(MDA) reactivity. RESULTS: 1) The MDA resctivity of erytbrocyte membrane in melatonin-treated diabetic animals (meanstandard deviation: 5.52+-1.52nmol/ml packed cells) were lower(p<0.05) than that in diabetic controls(7.68+-1.16nmol/mL packed cells). But, there was no significant difference between melatonin-treated diabetic animals and normal contls(4.93+-1.19 nmol/mL packed cells). 2) There were no significant differences of blood glucose and body weight between diabetic controls and melatonin-treated diabetic animals. CONCLUSION: These results show the antioxidative effect of melatonin in streptozotocin-induced diabetic rats. Further clinical and long-term experimental studies are needed to assess the effect of melatonin on development and progression of diabetic complications.