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Acta Physiologica Congress

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Acta Physiologica 2007; Volume 191, Supplement 658
Joint Meeting of The Slovak Physiological Society, The Physiological Society and The Federation of European Physiological Societies
9/11/2007-9/14/2007
Bratislava, Slovakia


BENEFICIAL EFFECT OF SODIUM SELENATE ON VASCULAR DYSFUNCTION IN DIABETIC RATS
Abstract number: PF18-150

Zeydanli1 E.N., Tanriverdi1 E., Seymen1 A., Tuncay1 E., Gurdal1 H., Koksoy1 A., Turan1 B.

1Dept. of Biophysics, Ankara University, Turkey [email protected]

Aims: 

Since selenium compounds can restore some metabolic parametersand structural alterations of diabetic rat tissues, we tempted to investigate whether these beneficial effects extend to the diabetic rat isolated thoracic aorta dysfunctions.

Methods: 

Diabetes was induced by streptozotocin (50 mg/kg body weight) and rats were treated with sodium selenate (15 mmol/kg body weight/day) for 4 weeks.

Results: 

Sodium selenate treatment of diabetic rats induced a significant recovery (80% wrt diabetes) in the depressed phenylephrine (10-8–10-5 M) stimulated isometric contractions(50% wrt control) in aorta while we obtained 100% recovery in the depressed relaxation responses (30% wrt control) with isoproterenol (10-9–10-4 M) without any significant changes in Log50 values. Sodium selenate treatment of the diabetic rats also restored the altered activities of several antioxidants enzymes of which are involved in the glutathione metabolism of the heart as well as the levels of glutathione and oxidized protein sulfhydryls while no significant effect on high blood glucose level. Our data indicate that anoxidant shift of cellular thiolic pools can modulate contraction-relaxationactivities of thoracic aorta in diabetic rats.

Conclusion: 

It can be summarizedthat selenium employs important roles in altered contraction-relaxationactivities of thoracic aorta via affecting the glutathione redox cycle to combatoxidative stress in diabetes and small doses of selenium compounds may beuseful as an adjunctive therapy in human diabetes.

To cite this abstract, please use the following information:
Acta Physiologica 2007; Volume 191, Supplement 658 :PF18-150

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