High
blood glucose concentration in diabetes induces
free radical production and, thus, causes oxidative stress. Damage of cellular structures by
free radicals play an important role in development of
diabetic complications. In this study, we evaluated effects of
sodium tungstate on enzymatic and nonenzymatic markers of oxidative stress in brain of
streptozotocin (STZ)-induced diabetic rats. Rats were divided into four groups (ten rats in each group): untreated control,
sodium tungstate-treated control, untreated diabetic, and
sodium tungstate-treated diabetic. Diabetes was induced with an intraperitoneal STZ injection (65 mg/kg
body weight), and
sodium tungstate with concentration of 2 g/L was added to
drinking water of treated animals for 4 weeks. Diabetes caused a significant increase in the brain
thiobarbituric acid reactive substances (P < 0.01) and
protein carbonyl levels (P < 0.01) and a decrease in ferric reducing
antioxidant power (P < 0.01). Moreover, diabetic rats presented a reduction in brain
glucose-6-phosphate dehydrogenase (21%),
superoxide dismutase (41%),
glutathione peroxidase (19%), and
glutathione reductase (36%) activities.
Sodium tungstate reduced the
hyperglycemia and restored the diabetes-induced changes in all mentioned markers of oxidative stress. However,
catalase activity was not significantly affected by diabetes (P = 0.4), while
sodium tungstate caused a significant increase in
enzyme activity of treated animals (P < 0.05). Data of present study indicated that
sodium tungstate can ameliorate brain oxidative stress in STZ-induced diabetic rats, probably by reducing of the high
glucose-induced oxidative stress and/or increasing of the
antioxidant defense mechanisms.