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The effects of di(2‐ethylhexyl)phthalate on rat liver in relation to selenium status
Author(s) -
Erkekoglu Pınar,
Zeybek Naciye D.,
Giray Belma K.,
Rachidi Walid,
Kızılgün Murat,
HiningerFavier Isabelle,
Favier Alain,
Asan Esin,
Hincal Filiz
Publication year - 2014
Publication title -
international journal of experimental pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.671
H-Index - 72
eISSN - 1365-2613
pISSN - 0959-9673
DOI - 10.1111/iep.12059
Subject(s) - phthalate , glutathione peroxidase , lipid peroxidation , chemistry , glutathione reductase , endocrinology , medicine , superoxide dismutase , selenium , catalase , glutathione , oxidative stress , antioxidant , biochemistry , biology , enzyme , organic chemistry
Summary 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 ( GP x1), glutathione peroxidase 4 ( GP x4), 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 GP x4 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.