RESUMO
Hyperglycemia-induced oxidative stress makes an important contribution to the etiology of diabetic teratogenicity namely fetal growth and congenital dysmorphogenesis. The aim of this study is to evaluate the protective roles of melatonin and insulin against diabetic's embryolethality and teratogenicity. Diabetes was induced to virgin Sprague Dawley albino rats by a single peritoneal injection of alloxan. Thirty pregnant rats were divided equally into 5 groups: 1) Control 2) Diabetic 3) Diabetic insulin 4) Diabetic melatonin 5) Diabetic melatonin-insulin. Insulin and melatonin were administered daily throughout the whole gestational period. Fetuses were collected on day 20 of gestation and were examined for malformations and growth disorders. A significant increase in fetal growth parameters (Macrosomia) were noticed in the diabetic group compared to the control. Melatonin prevents the appearance of soft tissue anomalies, but it leads to fetal growth restriction of diabetic rats (Microsomia). No significant changes were noticed in fetal growth parameters in diabetic insulin or in diabetic melatonin-insulin groups compared to the control. Congenital anomalies were not seen in diabetic insulin and in diabetic melatonin-insulin groups while the rate of resorption was reduced in both groups when compared to the diabetic group. In conclusion, co-administration of melatonin with insulin leads to a slight non significant improvement of the protective role of insulin against diabetic embryolethality, teratogenicity and fetal growth changes.