The effects of di(2-ethylhexyl)phthalate on rat liver in relation to selenium status
International Journal of Experimental Pathology, vol.95, no.1, pp.64-77, 2014 (SCI-Expanded, Scopus)
- Publication Type: Article / Article
- Volume: 95 Issue: 1
- Publication Date: 2014
- Doi Number: 10.1111/iep.12059
- Journal Name: International Journal of Experimental Pathology
- Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
- Page Numbers: pp.64-77
- Keywords: antioxidant enzymes, di(ethylhexyl)phthalate, liver, oxidative stress, selenium deficiency, selenium supplementation, OXIDATIVE STRESS, PEROXISOME PROLIFERATION, GLUTATHIONE-PEROXIDASE, NONGENOTOXIC CARCINOGENESIS, HEPATOCELLULAR-CARCINOMA, MAMMALIAN THIOREDOXIN, ANTIOXIDANT ENZYMES, SPECIES-DIFFERENCES, DIETARY SELENIUM, PHTHALATE DEHP
- Open Archive Collection: AVESIS Open Access Collection
- Lokman Hekim University Affiliated: No
Abstract
This study was performed to determine the hepatotoxicity of di(2-ethylhexyl)phthalate (DEHP) in relation to selenium status. In 3-week-old Sprague-Dawley rats, selenium deficiency was induced by a ≤0.05 selenium mg/kg. A selenium supplementation group was given 1 mg selenium/kg diet for 5 weeks. Di(2-ethylhexyl)phthalate-treated groups received 1000 mg/kg dose by gavage during the last 10 days of the experiment. Histopathology, peroxisome proliferation, catalase (CAT) immunoreactivity and activity and apoptosis were assessed. Activities of antioxidant selenoenzymes [glutathione peroxidase 1 (GPx1), glutathione peroxidase 4 (GPx4), thioredoxin reductase (TrxR1)], superoxide dismutase (SOD), and glutathione S-transferase (GST); aminotransferase, total glutathione (tGSH), and lipid peroxidation (LP) levels were measured. Di(2-ethylhexyl)phthalate caused cellular disorganization while necrosis and inflammatory cell infiltration were observed in Se-deficient DEHP group (DEHP/SeD). Catalase activity and immunoreactivity were increased in all DEHP-treated groups. Glutathione peroxidase 1 and GPx4 activities decreased significantly in DEHP and DEHP/SeD groups, while GST activities decreased in all DEHP-exposed groups. Thioredoxin reductase activity increased in DEHP and DEHP/SeS, while total SOD activities increased in all DEHP-treated groups. Lipid peroxidation levels increased significantly in SeD (26%), DEHP (38%) and DEHP/SeD (71%) groups. Selenium supplementation partially ameliorated DEHP-induced hepatotoxicity; while in DEHP/SeD group, drastic changes in hepatic histopathology and oxidative stress parameters were observed. International Journal of Experimental Pathology © 2014 International Journal of Experimental Pathology.