RESUMO
OBJECTIVES: Diabetes mellitus is associated with oxidative stress that leads to inflammation and diabetic nephropathy. This study aimed to determine the possible renoprotective effects of the antioxidants melatonin, vitamin D and vitamin E in diabetic rats. METHODS: We divided 108 albino rats into 12 groups. G1 group was fed a normal diet and did not receive any medication. G2 to G4 consisted of non-diabetic rats that were treated as follows: G2 with melatonin; G3 with vitamin E; G4 with vitamin D. Groups G5 to G12 consisted of diabetic rats that were treated as follows: G5 received no medication; G6 treated with insulin; G7 treated with melatonin; G8 treated with melatonin and insulin; G9 treated with vitamin E; G10 treated with vitamin E and insulin; G11 treated with vitamin D and G12 treated with vitamin D and insulin. Two months after treatment commenced, histological and biochemical examinations of glucose profile, oxidative stress status, renal function, homocysteine and TNF-α were performed. RESULTS: Total antioxidant capacity (TAC) increased significantly in groups G2, 7, 8, 10 and 11. TNF-α significantly increased in G2, but decreased in all other groups. Creatinine increased significantly in groups G5, 6, 7, 8, 9, 11 and 12. In the kidneys of the diabetic rats, thickened capillary basement membrane, diffuse mesangial sclerosis and nodular glomerulosclerosis was observed. Rats treated with melatonin showed marked improvement in these symptoms. However, in those treated with vitamin D and E, thickened capillary basement membrane and mesangial sclerosis was still present. CONCLUSIONS: Melatonin, administered either with or without insulin had a significant biochemical antioxidant effect and histological renoprotective effect. Conversely, vitamin D and E did not appear to have any effects on the parameters measured.
RESUMO
BACKGROUND: Diabetes mellitus (DM) is a serious chronic disease, with multiple complications including hepatopathy associated with imbalance of the oxidative status. The purpose of this study is to observe possible protective effects of vitamin-D and melatonin on glucose profile, antioxidant-oxidant status, lipid peroxidation, and histopathological protection of the liver in streptozotocin-induced diabetic rats. METHODS: Eighty three male albino rats were divided into nine groups as follows: G1 (n = 10) Normal control rats; G2 (n = 8) were normal rats treated with melatonin only; G3 (n = 10) were normal rats treated with vitamin D only; G4 (n = 9) were diabetic rats, which received no medications; G5 (n = 8) were diabetic rat treated with insulin only; G6 (n = 10) were diabetic rats treated with melatonin only; G7 (n = 9) were diabetic rats treated with melatonin and insulin; G8 (n = 9) were diabetic rats treated with vitamin D only; G9 (n = 10) were diabetic rats treated with vitamin D and insulin. Two months post treatment, blood was collected to measure: Fasting blood sugar (FBS), glycosylated hemoglobin (HbA1c), fructosamine (FA), total antioxidant capacity (TAC), malondialdahyde (MDA). livers were isolated for histopathological study. RESULTS: As compared to normal rats, our results demonstrate that glucose, fructosamine and HbA1c levels is increased in diabetic groups and declined to lesser levels in treated groups. TAC level of diabetic rats is not significantly changed. Vitamin D administration significantly increased TAC while it is not changed with melatonin either in treated or non-treated groups. The liver of diabetic rats shows only mild focal microvesicular fatty degeneration. The liver of diabetic rats treated with insulin shows degeneration of cell edema in the stroma. The liver of diabetic rats treated with melatonin with or without insulin, exhibited marked improvement. The liver of diabetic rats treated with vitamin D with or without insulin, shows degeneration of cells and edema in the stroma. CONCLUSION: Our results demonstrated the beneficial antioxidant effect of vitamin D administration to normal and diabetic rats as compared to melatonin. Nevertheless, melatonin still shows more therapeutic effect on liver cell injury induced by induction of diabetes.