The role of melatonin on uteroplacental antioxidant enzymes activities and fetal growth retardation in diabetic rats (910.1)

Abstract

Melatonin is an endogenous substance produced by the mammalian pineal gland and other organs. It is known to have antioxidant, antiaging and anticancer effects. The aim of the study was to investigate the effect of oral melatonin on fetal growth retardation, uteroplacental antioxidant enzymes activities and lipid peroxidation in experimental diabetic rats. Twenty pregnant rats were divided into four groups of five rats each. Diabetes mellitus was induced by intraperitoneal administration of 120mg/kg body weight of alloxan in groups 2, 3 and 4. From gestational day 1 to 19, 1mg/kg and 10mg/kg of oral melatonin were administered to the rats in groups 3 and 4. On the 19th day of gestation, the rats were sacrificed by cervical dislocation and placental, fetal and uterine tissues were harvested. In the harvested tissues, glutathione peroxidase (GPx), Superoxide dismutase (SOD), Catalase (CAT) and malondialdehyde (MDA) were estimated. In addition, fetal weight, fetal size and plasma glucose were determined. Our results showed that, in diabetic rats, fetal growth retardation was associated with a significant reduction in placental and uterine antioxidant enzymes (GPx, SOD and CAT) activities (P less than 0.01) and an increase in lipid peroxidation, MDA concentration (P less than 0.01). Treatment with oral melatonin improved the fetal weight, placental and uterine antioxidant enzymes activities and reduced lipid peroxidation, without affecting the degree of hyperglycemia. Our study has shown that reduced uteroplacental antioxidant enzyme activities and increased lipid peroxidation could be other sources of fetal growth retardation in diabetic rats. In conclusion, oral administration of melatonin to pregnant diabetic rats improved fetal growth. This effect seems to depend on the ability of melatonin to improve uteroplacental antioxidant enzymes activities and reduced lipid peroxidation.