title: Ozone oxidative preconditioning protects the rat kidney from reperfusion injury: the role of nitric oxide.
abstract: BACKGROUND
  Ischemia/reperfusion (I/R) injury, which is commonly seen in the field of renal surgery or transplantation, is a major cause of acute renal failure. Previous studies have shown that ozone oxidative preconditioning (OzoneOP) attenuated renal I/R injury. The objective of this study was to examine the hypothesis that protective effects of OzoneOP in renal I/R injury were associated with endogenous NO.
  
  
  METHODS
  In a right-nephrectomized rat mode, anesthetized rats underwent 45 min of renal ischemia. OzoneOP (1 mg/kg) was administered before I/R injury. Rats were killed at 24, 48, and 72 h after I/R injury and blood samples and renal tissues were obtained.
  
  
  RESULTS
  OzoneOP prevented the renal dysfunction induced by I/R and increased nitric oxide (NO) release and renal NO synthase (endothelial, eNOS, and inducible, iNOS) expression. In contrast, enhancement of endothelin-1 in the kidney after the reperfusion was markedly suppressed by OzoneOP.
  
  
  CONCLUSIONS
  Our findings indicated that the protective effect of OzoneOP was closely related to the NO production following the increase in eNOS and iNOS expression. Ozone treatment may have important clinical implications, particularly in view of the minimizing renal damage before transplantation.
authors.affiliation: Department of Urology, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, China.
authors.forename: Hui
authors.initials: H
authors.lastname: Chen
authors.forename: Bianzhi
authors.initials: B
authors.lastname: Xing
authors.forename: Xiuheng
authors.initials: X
authors.lastname: Liu
authors.forename: Bingyan
authors.initials: B
authors.lastname: Zhan
authors.forename: Jiangqiao
authors.initials: J
authors.lastname: Zhou
authors.forename: Hengcheng
authors.initials: H
authors.lastname: Zhu
authors.forename: Zhiyuan
authors.initials: Z
authors.lastname: Chen
mesh_terms: D058186:Acute Kidney Injury / Q000097:blood / Q000209:etiology / Q000517:prevention & control*; D000818:Animals; D001806:Blood Urea Nitrogen; D003404:Creatinine / Q000097:blood; D019332:Endothelin-1 / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D006146:Guanidines / Q000494:pharmacology; D019194:Ischemic Preconditioning; D007668:Kidney / Q000378:metabolism / Q000473:pathology; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000097:blood*; D052247:Nitric Oxide Synthase Type II / Q000037:antagonists & inhibitors / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III / Q000037:antagonists & inhibitors / Q000378:metabolism; D010126:Ozone / Q000627:therapeutic use*; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000097:blood / Q000150:complications / Q000473:pathology / Q000517:prevention & control*; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D019332:Endothelin-1; D006146:Guanidines; D009569:Nitric Oxide; D008315:Malondialdehyde; D010126:Ozone; D003404:Creatinine; D005979:Glutathione Peroxidase; D052247:Nitric Oxide Synthase Type II; D052250:Nitric Oxide Synthase Type III; D013482:Superoxide Dismutase; D005978:Glutathione; C004479:pimagedine; D019331:NG-Nitroarginine Methyl Ester