title: Borax partially prevents neurologic disability and oxidative stress in experimental spinal cord ischemia/reperfusion injury.
abstract: OBJECTIVE
  The aim of this study is to investigate the potential effects of borax on ischemia/reperfusion injury of the rat spinal cord.
  
  
  METHODS
  Twenty-one Wistar albino rats were divided into 3 groups: sham (no ischemia/reperfusion), ischemia/reperfusion, and borax (ischemia/reperfusion + borax); each group was consist of 7 animals. Infrarenal aortic cross clamp was applied for 30 minutes to generate spinal cord ischemia. Animals were evaluated functionally with the Basso, Beattie, and Bresnahan scoring system and inclined-plane test. The spinal cord tissue samples were harvested to analyze tissue concentrations of nitric oxide, nitric oxide synthase activity, xanthine oxidase activity, total antioxidant capacity, and total oxidant status and to perform histopathological examination.
  
  
  RESULTS
  At the 72nd hour after ischemia, the borax group had significantly higher Basso, Beattie, and Bresnahan and inclined-plane scores than those of ischemia/reperfusion group. Histopathological examination of spinal cord tissues in borax group showed that treatment with borax significantly reduced the degree of spinal cord edema, inflammation, and tissue injury disclosed by light microscopy. Xanthine oxidase activity and total oxidant status levels of the ischemia/reperfusion group were significantly higher than those of the sham and borax groups (P < .05), and total antioxidant capacity levels of borax group were significantly higher than those of the ischemia/reperfusion group (P < .05). There was not a significantly difference between the sham and borax groups in terms of total antioxidant capacity levels (P > .05). The nitric oxide levels and nitric oxide synthase activity of all groups were similar (P > .05).
  
  
  CONCLUSIONS
  Borax treatment seems to protect the spinal cord against injury in a rat ischemia/reperfusion model and improve neurological outcome.
authors.affiliation: Faculty of Medicine, Department of Neurology, Balıkesir University, Balıkesir, Turkey. Electronic address: erabiakoc@yahoo.com.
authors.forename: Emine Rabia
authors.initials: ER
authors.lastname: Koc
authors.affiliation: Faculty of Medicine, Department of Neurosurgery, Turgut Özal University, Ankara, Turkey.
authors.forename: Emre Cemal
authors.initials: EC
authors.lastname: Gökce
authors.affiliation: Faculty of Medicine, Department of Neurosurgery, Balıkesir University, Balıkesir, Turkey.
authors.forename: Mehmet Akif
authors.initials: MA
authors.lastname: Sönmez
authors.affiliation: Faculty of Medicine, Department of Biochemistry, Turgut Özal University, Ankara, Turkey.
authors.forename: Mehmet
authors.initials: M
authors.lastname: Namuslu
authors.affiliation: Department of Pathology, Ministry of Health, Dışkapı Yıldırım Beyazıt Education and Research Hospital, Ankara, Turkey.
authors.forename: Aysun
authors.initials: A
authors.lastname: Gökce
authors.affiliation: Faculty of Medicine, Department of Public Health and Medical Statistics, Balıkesir University, Balıkesir, Turkey.
authors.forename: A Said
authors.initials: AS
authors.lastname: Bodur
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D001881:Borates / Q000627:therapeutic use*; D008124:Locomotion / Q000187:drug effects; D008297:Male; D009422:Nervous System Diseases / Q000209:etiology* / Q000473:pathology / Q000517:prevention & control*; D018696:Neuroprotective Agents / Q000627:therapeutic use*; D009569:Nitric Oxide / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000150:complications* / Q000473:pathology; D020760:Spinal Cord Ischemia / Q000209:etiology* / Q000473:pathology / Q000517:prevention & control*; D014969:Xanthine Oxidase / Q000378:metabolism
chemical_list: D000975:Antioxidants; D001881:Borates; D018696:Neuroprotective Agents; C018851:borax; D009569:Nitric Oxide; D014969:Xanthine Oxidase
keywords: Borax; ischemia; neuroprotection; oxidative stress; reperfusion injury; spinal cord