Taurine supplementation restores antioxidant status and hepatic membrane-bound enzymes in streptozotocin-induced diabetic rats
Introduction and Aim: Chronic hyperglycemia in diabetes causes cellular damage through increased lipid peroxidation and reduced levels of antioxidants. The activities of membrane-bound enzymes are affected by oxidative stress. Taurine, a sulfur containing amino acid is shown to have hypoglycemic act...
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Veröffentlicht in: | Biomedicine 2020-11, Vol.39 (2), p.263-267 |
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Format: | Artikel |
Sprache: | eng |
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Zusammenfassung: | Introduction and Aim: Chronic hyperglycemia in diabetes causes cellular damage through increased lipid peroxidation and reduced levels of antioxidants. The activities of membrane-bound enzymes are affected by oxidative stress. Taurine, a sulfur containing amino acid is shown to have hypoglycemic activity, antioxidant property and membrane stabilization. The aim of the study is to check the effect of supplementation of taurine on lipid peroxidation, antioxidant status and hepatic membrane-bound enzymes in streptozotocin- induced diabetic rats.
Materials and Methods: Thirty-two Wistar male albino rats of 19±1 weeks of age weighing 200-220 grams were randomly divided into four groups and each group consisted of eight animals. Group I (control) standard chow diet; Group II (chow diet with taurine); Group III (diabetes induced) and Group IV (diabetic receiving taurine). At the end of 45th day, all animals were sacrificed by cervical decapitation after overnight fasting. Blood and liver tissue samples were collected. The levels of glucose in plasma and lipid peroxidation, antioxidants and the activities of Na+/ K+, Ca2+ and Mg2+-ATPases in liver homogenate were analyzed.
Results: Altered levels of antioxidants and activities of Na+/ K+, Ca2+ and Mg2+-ATPases were restored to normal by taurine supplementation in diabetic rats.
Conclusion: The present study indicates that supplementation of taurine could protect liver plasma membrane against oxidative damage by acting as antioxidant and restoring the normal activities of Na+/ K+, Ca2+ and Mg2+-ATPases.
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ISSN: | 0970-2067 |
DOI: | 10.51248/.v39i2.192 |