Abstract

Accumulation of reactive oxygen species resulting from hyperglycemia and inadequate endogenous antioxidants are responsible for the complications of diabetes. Accumulation of reactive oxygen species in the cells stimulates apoptosis, which hampers the cell architecture and functions of vital organs. This study investigates the effect of fucoidan from Sargassum wightii, a potent antioxidant with a regulatory effect on blood glucose homeostasis, in the liver and kidney of diabetic rats. Diabetes was induced in rats by administrating streptozotocin 50 mg/kg for 3 consecutive days through intraperitoneal injection. 30 male Wistar rats were divided into five groups consisting of six animals in each group and they were Group A: Control group, Group B: Diabetic group, Group C: Diabetic rats treated with metformin hydrochloride 250 mg/kg, Group D: Diabetic rats treated with fucoidan 50 mg/kg, and Group E: Diabetic rats treated with fucoidan 100 mg/kg. Fucoidan was administrated orally for 4 w after the induction of diabetes. Superoxide dismutase activity was low in the liver of the diabetic group and it showed 58.5 % activity, compared with the control group. Fucoidan administration elevated superoxide dismutase and it was 66.5 % and 80.6 % respectively in fucoidan 50 mg/kg and fucoidan 100 mg/kg groups, compared with the control group while in the metformin group 93.4 % activity was seen. A similar variation in the superoxide dismutase was observed in the kidney; wherein, administration of fucoidan restored the superoxide dismutase activity and it was 62.9 % in the fucoidan 50 mg/kg group and 79.5 % in the fucoidan 100 mg/kg group, compared with the control group while in diabetic group 49.4 % and metformin group 94.2 % activity were observed. The other tested antioxidant enzymes such as catalase, glutathione peroxidase and glutathione S transferase also showed marked regain in a dose-dependent manner upon administration of fucoidan. This study inferred that the administration of fucoidan in streptozotocininduced diabetic rats improved the antioxidant enzyme activity by moderating the accumulation of reactive oxygen species and reduced the pathophysiology.