Sodium selenite protects against diabetes-induced alterations in the antioxidant defense system of the liver

Ayaz M., Celik H. A., AYDIN H. H., TURAN B.

Diabetes/Metabolism Research and Reviews, cilt.22, sa.4, ss.295-299, 2006 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 22 Sayı: 4
  • Basım Tarihi: 2006
  • Doi Numarası: 10.1002/dmrr.601
  • Dergi Adı: Diabetes/Metabolism Research and Reviews
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.295-299
  • Anahtar Kelimeler: oxidative stress, lipid peroxidation, superoxide dismutase, glutathione peroxidase, glutathione reductase, total glutathione, metallothionein, THIOREDOXIN REDUCTASE-ACTIVITY, GLUTATHIONE-PEROXIDASE, OXIDATIVE STRESS, METALLOTHIONEIN, SUPEROXIDE
  • Lokman Hekim Üniversitesi Adresli: Hayır

Özet

Background: Free radical genesis of disorder is one of the major subjects of discussion in the explanation of pathological conditions. In this study, the effects of micro molar quantities of sodium selenite treatment on diabetes-induced alterations in the antioxidant defense system were investigated. Methods: Diabetes was induced by administration of streptozotocin (STZ, 50 mg/kg body weight) and both diabetic and control animals were treated with sodium selenite (5 μmol/kg/day) for 4 weeks. Results: Our results have shown that induction of diabetes in the liver tissue of animals for 5 weeks resulted in decreased superoxide dismutase (SOD), glutathione reductase (GR) and glutathione peroxidase (GSHPx) activities and concomitantly increased lipid peroxidation (LPO). Conclusion: Sodium selenite treatment of the diabetic rats resulted in almost full restoration of all the parameters mentioned above. Metallothionein, which is known to be one of the major antioxidants and a central protein in heavy metal regulation, is altered by diabetes, and sodium selenite treatment restored this alteration as well. Copyright © 2005 John Wiley & Sons, Ltd.