Mercuric chloride induced hepatotoxic and hematologic changes in rats: The protective effects of sodium selenite and vitamin E


UZUNHİSARCIKLI M., ASLANTÜRK A., KALENDER S., APAYDIN F. G., BAŞ H.

TOXICOLOGY AND INDUSTRIAL HEALTH, cilt.32, sa.9, ss.1651-1662, 2016 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 32 Sayı: 9
  • Basım Tarihi: 2016
  • Doi Numarası: 10.1177/0748233715572561
  • Dergi Adı: TOXICOLOGY AND INDUSTRIAL HEALTH
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.1651-1662
  • Anahtar Kelimeler: Mercuric chloride, sodium selenite, vitamin E, histopathology, oxidative stress, hepatotoxicity, ANTIOXIDANT DEFENSE SYSTEM, INDUCED OXIDATIVE STRESS, BIOCHEMICAL PARAMETERS, LIPID-PEROXIDATION, INORGANIC MERCURY, REPRODUCTIVE TOXICITY, LIVER, CADMIUM, EXPOSURE, DAMAGE
  • Yozgat Bozok Üniversitesi Adresli: Evet

Özet

This study focuses on investigating the possible protective effect of sodium selenite (Na2SeO3) and/or vitamin E against mercuric chloride (HgCl2)-induced hepatotoxicity in rat. Male rats were given HgCl2 ( I mg/kg body weight (bw)) and HgCl2 plus Na2SeO3 (0.25 mg/kg bw) and/or vitamin E (100 mg/kg bw) daily via gavage for 4 weeks. HgCl2-treated groups had significantly higher white blood cell and thrombocyte counts than the control group. Serum activities of alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, gamma-glutamyl-transferase, and lactate dehydrogenase significantly increased and serum levels of total protein, albumin, triglyceride, total cholesterol, and low-density lipoprotein cholesterol significantly decreased in the HgCl2-treated groups compared with control group. Malondialdehyde level significantly increased and superoxide dismutase, catalase, and glutathione peroxidase activities decreased in liver tissue of HgCl2-treated rats. Also, HgCl2 exposure resulted in histopathological changes. Supplementation of Na2SeO3 and/or vitamin E provided partial protection in hematological and biochemical parameters that were altered by HgCl2. As a result, Na2SeO3 and/or vitamin E significantly reduced HgCl2-induced hepatotoxicity, but not protected completely.