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   <subfield code="a">Hesperidin ameliorates trichloroethylene-induced nephrotoxicity by abrogation of oxidative stress and apoptosis in wistar rats</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Aisha Siddiqi, Sana Nafees, Summya Rashid, Sarwat Sultana, Bano Saidullah]</subfield>
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   <subfield code="a">Trichloroethylene (TCE), a nephrotoxicant is known to cause severe damage to the kidney. In this study, the nephroprotective potential of hesperidin was evaluated against TCE-induced nephrotoxicity in wistar rats. Oral administration of TCE (1000mg/kg b.wt) for 15days enhanced renal lipid peroxidation and reduced antioxidant enzymes armoury viz., reduced renal glutathione, glutathione peroxidase, glutathione reductase, glutathione-S-transferase, catalase and superoxide dismutase. It also enhanced the levels of blood urea nitrogen, creatinine and kidney injury molecule (KIM-1). Caspase-3 and bax expression were found to be elevated, while that of bcl-2 reduced suggesting that TCE induces apoptosis. However, pretreatment with hesperidin at a dose of 100 and 200mg/kg b.wt for 15days significantly decreased lipid peroxidation, increased the levels of antioxidant enzymes and reduced blood urea, creatinine and KIM-1 levels. Hesperidin also modulated the apoptotic pathways by altering the expressions of caspase-3, bax and bcl-2 to normal. Our results suggest that hesperidin can be used as a nephroprotective agent against TCE-induced nephrotoxicity. Graphical Abstract:</subfield>
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   <subfield code="a">Springer Science+Business Media New York, 2015</subfield>
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   <subfield code="a">Trichloroethylene</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">Nephrotoxicity</subfield>
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   <subfield code="a">Hesperidin</subfield>
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   <subfield code="a">Oxidative stress</subfield>
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   <subfield code="a">Apoptosis</subfield>
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   <subfield code="a">TCE : 1,1,2-Trichloroethylene</subfield>
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   <subfield code="a">DCVG : S-(1,2-dichlorovinyl)-l-glutathione</subfield>
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   <subfield code="a">DCVC : S-(1,2-dichlorovinyl)-l-cysteine</subfield>
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   <subfield code="a">GPx : Glutathione peroxidase</subfield>
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   <subfield code="a">GSH : Glutathione</subfield>
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   <subfield code="a">GR : Glutathione reductase</subfield>
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   <subfield code="a">LPO : Lipid peroxidation</subfield>
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   <subfield code="a">MDA : Malondialdehyde</subfield>
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   <subfield code="a">PMS : Post-mitochondrial supernatant</subfield>
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   <subfield code="a">SOD : Superoxide dismutase</subfield>
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   <subfield code="a">BUN : Blood urea nitrogen</subfield>
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   <subfield code="a">KIM-1 : Kidney injury molecule</subfield>
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   <subfield code="a">HS : Hesperidin</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">ROS : Reactive oxygen species</subfield>
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   <subfield code="u">Section of Molecular Carcinogenesis and Chemoprevention, Department of Medical Elementology and Toxicology, Faculty of Science, Jamia Hamdard (Hamdard University), Hamdard Nagar, 110062, New Delhi, India</subfield>
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   <subfield code="t">Molecular and Cellular Biochemistry</subfield>
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   <subfield code="a">Metadata rights reserved</subfield>
   <subfield code="b">Springer special CC-BY-NC licence</subfield>
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