Assessment of susceptibility of different areas of brain to oxidative stress in insulin induced hypoglycaemic diabetic rats

Authors:S.Datta, M.Pal, U.K.Roy, T.Ghosh, S.Harlalka, A.Ray Chaudhuri
Int J Biol Med Res. 2013; 4(4): 3550-3557  |  PDF File

Abstract

Background: Both chronic hyperglycemias and acute hypoglycaemia in Diabetes seems to potentiates oxidative stress perhaps contributing to neural injury particularly in brain. Damages of brain caused by alteration of blood glucose do not uniform throughout the brain. So, aim of the present study was to locate the area of brain that is more susceptible to oxidative stress in chronic hyperglycemia and acute hypoglycaemia in diabetic rat brain model. Methods: The experiment was performed in male Wistar rats (n = 32). The rats were divided into three groups. In the first two groups diabetes was induced by a single intravenous injection of freshly prepared Streptozotocin (STZ) 60 mg kg/body weight. In the second group insulin was administered intraperitoneally (6.0 IU/Kg diluted in normal saline) after 10 days of diabetes induction. The third group served as the control. Then all rats from each group were sacrificed by cervical dislocation and the brain was segregated into cortex, cerebellum, midbrain and basal ganglia to estimate for malondialdehyde (MDA), protein carbonyls (PC) adducts, cytosolic superoxide dismutase (Cu2+-Zn2+-SOD) . Result: All the above areas showed significantly higher mean values for MDA and PC products with lower mean Cu2+-Zn2+-SOD activity in diabetic rats than controls. Significant another increase of these parameters occurred when insulin was administered to induced hypoglycaemia in above diabetic rats. confirmed that Oxidative stress markers were highest in the basal ganglia region compared to other brain areas (p < 0.001 for both MDA and PC products) in chronic hyperglycemia as well as acute hypoglycaemia in diabetes (Post hoc ANOVA). Conclusion: Basal ganglia is susceptible to oxidative stress induced injury in hyperglycemia and more in acute hypoglycemia of diabetic rats.