title: Medical ozone therapy reduces oxidative stress and intestinal damage in an experimental model of necrotizing enterocolitis in neonatal rats.
abstract: OBJECTIVE
  Necrotizing enterocolitis (NEC) remains a major cause of morbidity and death in neonates. Evidence suggests that an imbalance between activated proinflammatory response with inadequate antiinflammatory protection results in NEC. Ozone has been proposed as an antioxidant enzyme activator, immunomodulator, and cellular metabolic activator. Therefore, this study was designed to investigate whether medical ozone therapy is effective on neonatal rat model of NEC.
  
  
  METHODS
  Thirty-eight newborn Sprague-Dawley pups were randomly divided into 3 groups of NEC, NEC + ozone, and control (left to breast feed). Necrotizing enterocolitis was induced by enteral formula feeding and exposure to 100% carbon dioxide inhalation for 10 minutes after +4 degrees C cold exposures for 5 minutes and 97% oxygen for 5 minutes 2 times daily. The NEC + ozone group received 0.7 mg/kg per day ozone/oxygen mixture intraperitoneally for a total of 3 days after first day of NEC procedure. The pups were killed at fourth day, and their intestinal tissues were harvested for biochemical and histopathologic analysis. Blood sample from pups were also obtained.
  
  
  RESULTS
  The mortality rate and the weight loss were significantly higher in NEC group than control and treatment groups. Oxidative stress markers (malondialdehyde and protein carbonyl content) significantly increased and antioxidant enzyme activities (superoxide dismutase and glutathione peroxidase) were significantly decreased in NEC group. All these biochemical changes were ameliorated in NEC + ozone group. Nitrate plus nitrite levels and serum tumor necrosis factor alpha were elevated in NEC group and reduced in treatment group. In addition, histopathologic injury score of NEC group was significantly higher than NEC + ozone group.
  
  
  CONCLUSIONS
  Ozone treatment significantly reduced the severity of NEC by modulating antioxidative defense and antiinflammatory protection in our experimental animal model.
authors.affiliation: Department of Pediatric Surgery, Gulhane Military Medical Academy, Etlik, Ankara, Turkey. drahmetguven@yahoo.com
authors.forename: Ahmet
authors.initials: A
authors.lastname: Guven
authors.forename: Gokhan
authors.initials: G
authors.lastname: Gundogdu
authors.forename: Sabahattin
authors.initials: S
authors.lastname: Vurucu
authors.forename: Bulent
authors.initials: B
authors.lastname: Uysal
authors.forename: Emin
authors.initials: E
authors.lastname: Oztas
authors.forename: Haluk
authors.initials: H
authors.lastname: Ozturk
authors.forename: Ahmet
authors.initials: A
authors.lastname: Korkmaz
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D015415:Biomarkers / Q000097:blood*; D004195:Disease Models, Animal; D020345:Enterocolitis, Necrotizing / Q000188:drug therapy* / Q000401:mortality; D005979:Glutathione Peroxidase / Q000097:blood; D008315:Malondialdehyde / Q000097:blood; D009566:Nitrates / Q000097:blood; D009573:Nitrites / Q000097:blood; D010126:Ozone / Q000494:pharmacology*; D050050:Protein Carbonylation; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D018709:Statistics, Nonparametric; D013482:Superoxide Dismutase / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D015415:Biomarkers; D009566:Nitrates; D009573:Nitrites; D014409:Tumor Necrosis Factor-alpha; D008315:Malondialdehyde; D010126:Ozone; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase