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Adenosine triphosphatase activity of streptozotocin-induced diabetic rat brain microsomes. Effect of vitamin E
N Das Evcimen1, N N Ulusu, C Karasu
1Ankara University, Faculty of Pharmacy, Department of Biochemistry, Ankara, Turkey. evcimen@pharmacy.ankara.edu.tr
Abstract:
Hyperglycemia causes protein glycosylation, oxidation and alterations in enzyme activities, which are the underlying causes of diabetic complications. This study was undertaken to test the role of vitamin E treatment on Ca2+-ATPase activity, protein glycosylation and lipid peroxidation in the brain of streptozotocin (STZ)-induced diabetic rats. Male rats weighing about 250-300 g were rendered diabetic by a single STZ injection of 50 mg/kg via the tail vein. Both the diabetic and non-diabetic rats were fed a vitamin E supplemented diet (500 IU/kg/day). Ca2+-ATPase activity was significantly reduced at week 10 of diabetes compared to the control group (p < 0.05), with 0.225+/-0.021 U/I (mean +/- S.E.M.) in the control group and 0.072 +/- 0.008 U/l (mean +/- S.E.M.) in the diabetic group. Vitamin E treatment prevented the enzyme activity from decreasing. The activities observed were 0.226 +/- 0.020 U/l and 0.172 +/- 0.011 U/I (mean +/- S.E.M.) in the vitamin E-treated control and diabetic group, respectively. STZ-induced diabetes resulted in an increased protein glycosylation and lipid peroxidation. Vitamin E treatment led to a significant inhibition in blood glucose, protein glycosylation and lipid peroxidation, which in turn prevented abnormal activity of the enzyme in the brain. This study indicates that vitamin E supplementation may reduce complications of diabetes in the brain.
Insights
Vitamin E supplementation helps prevent diabetic complications in the brain by reducing high blood glucose, protein glycosylation, and lipid peroxidation. This treatment preserves Ca2+-ATPase enzyme activity in diabetic rats.
Area of Science:
- Biochemistry
- Neuroscience
- Endocrinology
Background:
- Hyperglycemia in diabetes leads to detrimental protein modifications and oxidative stress.
- These changes contribute to the development of diabetic complications, particularly in neural tissues.
- Ca2+-ATPase activity is crucial for neuronal function and is affected by diabetic conditions.
Purpose of the Study:
- To investigate the protective effects of vitamin E on brain biochemistry in streptozotocin-induced diabetic rats.
- To assess the impact of vitamin E on Ca2+-ATPase activity, protein glycosylation, and lipid peroxidation.
- To determine if vitamin E can mitigate diabetes-related alterations in the brain.
Main Methods:
- Diabetes was induced in male rats using streptozotocin (STZ).
- Diabetic and control rats were administered a vitamin E-supplemented diet.
- Ca2+-ATPase activity, protein glycosylation, and lipid peroxidation levels were measured in brain tissue.
Main Results:
- STZ-induced diabetes significantly reduced Ca2+-ATPase activity and increased protein glycosylation and lipid peroxidation.
- Vitamin E treatment normalized Ca2+-ATPase activity in diabetic rats.
- Vitamin E supplementation inhibited hyperglycemia, protein glycosylation, and lipid peroxidation, preserving enzyme function.
Conclusions:
- Vitamin E exhibits neuroprotective effects against hyperglycemia-induced damage in diabetic rats.
- Supplementation with vitamin E may be a viable strategy to reduce diabetic complications in the brain.
- The antioxidant and anti-glycation properties of vitamin E are key to its beneficial effects.
