Abstract
Since selenium compounds can restore some metabolic parameters and structural alterations of diabetic rat tissues, we tempted to investigate whether these beneficial effects extend to the diabetic rat isolated thoracic aorta dysfunctions. Diabetes was induced by streptozotocin (50 mg/kg body weight) and rats were treated with sodium selenate (15 μmol/kg body weight/ day) for 4 weeks. Sodium selenate treatment of diabetic rats induced a significant recovery (80% wrt diabetes) in the depressed phenylephrine (10–10 M) stimulated isometric contractions (50% wrt control) in aorta while we obtained 100% recovery in the depressed relaxation responses (30% wrt control) with isoproterenol (10–10 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 sulphydryls while no significant effect on high blood glucose level. Our data indicate that an oxidant shift of cellular thiolic pools can modulate contraction-relaxation activities of thoracic aorta in diabetic rats. Therefore, it can be summarized that selenium employs important roles in altered contraction-relaxation activities of thoracic aorta via affecting the glutathione redox cycle to combat oxidative stress in diabetes and small doses of selenium compounds may be useful as an adjunctive therapy in human diabetes.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.