title: Nephroprotective efficacy of chrysin against cisplatin-induced toxicity via attenuation of oxidative stress.
abstract: OBJECTIVE
  Cisplatin-induced nephrotoxicity is the main cause for its dose-limited use in the treatment of various cancers and results in acute renal cell injury through generation of reactive oxygen species. Chrysin possess antioxidant, anti-inflammatory and anti-cancer properties. The aim of this study was to investigate the protective efficacy of chrysin against cisplatin-induced nephrotoxicity.
  
  
  METHODS
  Thirty male Wistar rats were divided into five groups with six rats in each group. Group I served as control and received corn oil (vehicle of chrysin) for 14 days and 0.9% saline (vehicle of cisplatin) on day 14 only. Group II received a single intraperitoneal injection of cisplatin on day 14. Group III and IV were pretreated with two different doses of chrysin in addition to cisplatin and group V received chrysin only. Rats were examined for the effect of chrysin on cisplatin induced depletion of antioxidant enzymes, induction of lipid peroxidation and DNA damage in the kidney, utilizing a well-established model of cisplatin-induced nephropathy.
  
  
  RESULTS
  Pretreatment with chrysin significantly attenuated cisplatin-induced renal oxidative damage by diminishing the DNA damage and toxicity markers, such as creatinine and blood urea nitrogen, lipid peroxidation and xanthine oxidase activity, accompanied by increase in enzymatic (catalase, glutathione peroxidase, glutathione reductase and glutathione-S-transferase) and non-enzymatic (reduced glutathione) antioxidant status. Histological findings further substantiated the protective efficacy of chrysin, which reduced cisplatin-induced renal damage.
  
  
  CONCLUSIONS
  The data of the present study suggest that chrysin effectively suppress cisplatin-induced renal injury by ameliorating oxidative stress.
authors.affiliation: Molecular Carcinogenesis and Chemoprevention Division, Department of Medical Elementology and Toxicology, Faculty of Science, Jamia Hamdard-Hamdard University, Hamdard Nagar, New Delhi, India. sarwat786@rediffmail.com
authors.forename: Sarwat
authors.initials: S
authors.lastname: Sultana
authors.forename: Kriti
authors.initials: K
authors.lastname: Verma
authors.forename: Rehan
authors.initials: R
authors.lastname: Khan
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology / Q000627:therapeutic use; D000970:Antineoplastic Agents / Q000627:therapeutic use / Q000633:toxicity*; D000975:Antioxidants / Q000378:metabolism / Q000494:pharmacology / Q000627:therapeutic use*; D015415:Biomarkers / Q000097:blood; D001806:Blood Urea Nitrogen; D002945:Cisplatin / Q000627:therapeutic use / Q000633:toxicity*; D003404:Creatinine / Q000097:blood; D004249:DNA Damage / Q000187:drug effects; D005419:Flavonoids / Q000494:pharmacology / Q000627:therapeutic use*; D007668:Kidney / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D007674:Kidney Diseases / Q000188:drug therapy* / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D009369:Neoplasms / Q000188:drug therapy; D018384:Oxidative Stress / Q000187:drug effects*; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism; D012076:Renal Agents / Q000494:pharmacology / Q000627:therapeutic use; D014969:Xanthine Oxidase / Q000037:antagonists & inhibitors
chemical_list: D000893:Anti-Inflammatory Agents; D000970:Antineoplastic Agents; D000975:Antioxidants; D015415:Biomarkers; D005419:Flavonoids; D017382:Reactive Oxygen Species; D012076:Renal Agents; C043561:chrysin; D003404:Creatinine; D014969:Xanthine Oxidase; D002945:Cisplatin