title: Ozone oxidative post-conditioning in acute renal failure.
abstract: OBJECTIVE
  The ischaemia-reperfusion process is largely mediated by reactive oxygen species. Taking into account that a transient and controlled administration of ozone is able to upregulate cellular antioxidant enzymes, a morphological, biochemical and functional renal study was performed in rats undergoing warm renal ischaemia.
  
  
  METHODS
  Rats were divided into four groups. All except the negative controls underwent 60 min' bilateral renal ischaemia followed by 10 days' reperfusion. The positive control group received no further treatment. The ozone group received an ozone/oxygen mixture (ozone dose 0.5 mg/kg) immediately after the ischaemia and daily for the 10 days' reperfusion; the oxygen group were given the same concentration of oxygen alone (13 mg/kg). Biochemical parameters fructosamine, phospholipase A2, catalase, superoxide dismutase and thiobarbituric acid reactive substances were measured, as well as renal plasma flow and glomerular filtration rate.
  
  
  RESULTS
  Renal plasma flow and glomerular filtration rate decreased significantly in the positive controls and the oxygen group whereas values in the ozone group were similar to those in the negative control group. With respect to the biochemical parameters, ozone maintained a homeostasis redox, with significant increases in catalase and superoxide dismutase activities and similar values for phospholipase A2 and fructosamine compared with the negative control group. Fewer morphological alterations were seen in kidneys from the ozone group. No advantages were obtained in the positive control and oxygen groups.
  
  
  CONCLUSIONS
  The protective effect of ozone may be explained by upregulation of the antioxidant defence system and beneficial effects on blood circulation and in oxygen metabolism. Ozone treatment may represent a therapeutic approach for minimising renal damage after transplantation.
authors.affiliation: Ozone International Clinic, Ozone Research Center, Havana, Cuba.
authors.forename: José Luis
authors.initials: JL
authors.lastname: Calunga
authors.forename: Yanelis
authors.initials: Y
authors.lastname: Trujillo
authors.forename: Silvia
authors.initials: S
authors.lastname: Menéndez
authors.forename: Zullyt
authors.initials: Z
authors.lastname: Zamora
authors.forename: Yaima
authors.initials: Y
authors.lastname: Alonso
authors.forename: Nelson
authors.initials: N
authors.lastname: Merino
authors.forename: Teresa
authors.initials: T
authors.lastname: Montero
mesh_terms: D058186:Acute Kidney Injury / Q000175:diagnosis / Q000188:drug therapy* / Q000503:physiopathology; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology / Q000627:therapeutic use; D004195:Disease Models, Animal; D016166:Free Radical Scavengers / Q000037:antagonists & inhibitors / Q000378:metabolism; D019270:Fructosamine / Q000378:metabolism; D007668:Kidney / Q000187:drug effects; D007677:Kidney Function Tests; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D010100:Oxygen / Q000627:therapeutic use*; D010126:Ozone / Q000032:analysis / Q000627:therapeutic use*; D054467:Phospholipases A2 / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000494:pharmacology / Q000627:therapeutic use; D013482:Superoxide Dismutase / Q000037:antagonists & inhibitors / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances; D052096:Warm Ischemia
chemical_list: D000975:Antioxidants; D016166:Free Radical Scavengers; D017382:Reactive Oxygen Species; D017392:Thiobarbituric Acid Reactive Substances; D019270:Fructosamine; D010126:Ozone; D013482:Superoxide Dismutase; D054467:Phospholipases A2; D010100:Oxygen