Protective Effects of Sodium Selenite and Vitamin E on Mercuric Chloride-Induced Cardiotoxicity in Male Rats

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Karaboduk H., Uzunhisarcıklı M., Kalender Y.

BRAZILIAN ARCHIVES OF BIOLOGY AND TECHNOLOGY, cilt.58, sa.2, ss.229-238, 2015 (SCI-Expanded) identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 58 Sayı: 2
  • Basım Tarihi: 2015
  • Doi Numarası: 10.1590/s1516-8913201400339
  • Dergi Adı: BRAZILIAN ARCHIVES OF BIOLOGY AND TECHNOLOGY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.229-238
  • Anahtar Kelimeler: Mercuric chloride, Sodium selenite, Vitamin E, Cardiotoxicity, Oxidative Stress, OXIDATIVE STRESS, LIPID-PEROXIDATION, BIOCHEMICAL PARAMETERS, INORGANIC MERCURY, HEAVY-METALS, TOXICITY, ACID, CADMIUM, ANTIOXIDANTS, ERYTHROCYTES
  • Gazi Üniversitesi Adresli: Evet

Özet

This study was designed to investigate the protective effects of sodium selenite and/or vitamin E against mercuric chloride-induced cardiotoxicity. Male Wistar rats (n=48, 310 +/- 10 g) were administered mercuric chloride (1.0 mg/kg bw), sodium selenite (0.25 mg/kg bw), vitamin E (100 mg/kg bw), sodium selenite plus mercuric chloride, vitamin E plus mercuric chloride and sodium selenite plus vitamin E plus mercuric chloride daily via gavage for four weeks. Malondialdehyde (MDA) level, antioxidant enzyme activities [total superoxide dismutase (SOD), catalase (CAT), total glutathione peroxidase (GPx) and total glutathione-S-transferase (GST)], and histopathological changes in the heart tissue were evaluated. Results showed that mercuric chloride exposure resulted in an increase in the MDA level and a decrease in the SOD, CAT, GPx and GST activities, with respect to the control. Light microscopic investigations revealed that mercuric chloride induced histopathological changes in the heart tissue. A significant decrease in the MDA level and a significant increase in the SOD, CAT, GPx and GST activities were observed on the supplementation of sodium selenite and/or vitamin E to mercuric chloride-treated rats, which showed that, sodium selenite and/or vitamin E significantly reduced mercuric chloride induced cardiotoxicity, but not protected completely.