Sodium selenite and vitamin E in preventing mercuric chloride induced renal toxicity in rats

ASLANTÜRK A., Uzunhisarcikli M., KALENDER S., DEMİR F.

FOOD AND CHEMICAL TOXICOLOGY, cilt.70, ss.185-190, 2014 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 70
  • Basım Tarihi: 2014
  • Doi Numarası: 10.1016/j.fct.2014.05.010
  • Dergi Adı: FOOD AND CHEMICAL TOXICOLOGY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.185-190
  • Anahtar Kelimeler: Mercuric chloride, Sodium selenite, Vitamin E, Histopathology, Oxidative stress, Kidney toxicity, INDUCED OXIDATIVE STRESS, ANTIOXIDANT ENZYME-ACTIVITY, LIPID-PEROXIDATION, INDUCED NEPHROTOXICITY, PROTECTIVE ROLE, LIVER, CADMIUM, KIDNEY, ACID, LEAD
  • Gazi Üniversitesi Adresli: Evet

Özet

This study aims to investigate improving effects of sodium selenite and/or vitamin E on mercuric chloride-induced kidney impairments in rats. Wistar male rats were exposed either to sodium selenite (0.25 mg/kg day), vitamin E (100 mg/kg day), sodium selenite + vitamin E, mercuric chloride (1 mg/kg day), sodium selenite + mercuric chloride, vitamin E + mercuric chloride and sodium selenite + vitamin E + mercuric chloride for 4 weeks. Mercuric chloride exposure resulted in an increase in the uric acid, creatinine, blood urea nitrogen and malondialdehyde (MDA) levels and a decrease in the superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) activities. Histopathological changes were detected in kidney tissues in mercuric chloride-treated groups. A significant decrease in the uric acid, creatinine, blood urea nitrogen and MDA levels and a significant increase in the SOD, CAT and GPx activities were observed in the supplementation of sodium selenite and/or vitamin E to mercuric chloride-treated groups.