title: Activity of mannitol and hypertonic saline therapy on the oxidant and antioxidant system during the acute term after traumatic brain injury in the rats.
abstract: In this study, our objective is to investigate the effects of mannitol and 7.5% hypertonic saline (HS) therapy on the levels of malondialdehyde (MDA), catalase and glutathione peroxidase (GSH-Px) in the early stages of experimental head traumas in rats. Rats included in the study were divided into four groups: Group I Control, Group II Trauma, Group III Mannitol, and Group IV 7.5% Hypertonic Saline. Rats in Group II were subject to head trauma only. Mannitol was injected intraperitoneally to rats in Group III after head trauma and 7.5% HS was injected intraperitoneally to rats in Group IV after head trauma. Rats were sacrificed 4 h after administration of mannitol or 7.5% HS, and the levels of MDA catalase and GSH-Px in brain tissues extracted from rats were determined. MDA levels in the trauma group were significantly increased compared with the control group (p<0.01), whereas there was a reduction in catalase and GSH-Px levels, although these differences were not significant. By contrast, in the mannitol group, MDA, catalase and GSH-Px levels were lower than the levels in the trauma group, and these reductions were statistically significant (p<0.05). The MDA, catalase and GSH-Px levels of the 7.5% HS group were lower than those of the trauma group; however, this reduction was not statistically significant. It was concluded that mannitol and 7.5% HS therapies that are used to reduce intracranial pressure and to increase the use of catalase, an antioxidant enzyme, and GSH-Px, are likely to reduce cellular damage by reducing the formation of MDA, the levels of which are known to be indicative of cellular level oxidant damage.
authors.affiliation: Department of Neurosurgery, School of Medicine, Yuzuncu Yil University, Van, Turkey. yilmaznebi@yahoo.com
authors.forename: Nebi
authors.initials: N
authors.lastname: Yilmaz
authors.forename: Haluk
authors.initials: H
authors.lastname: Dulger
authors.forename: Nejmi
authors.initials: N
authors.lastname: Kiymaz
authors.forename: Cahide
authors.initials: C
authors.lastname: Yilmaz
authors.forename: Burhan O
authors.initials: BO
authors.lastname: Gudu
authors.forename: Ismail
authors.initials: I
authors.lastname: Demir
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D001921:Brain / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology; D001929:Brain Edema / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology; D001930:Brain Injuries / Q000150:complications / Q000503:physiopathology*; D002374:Catalase / Q000187:drug effects / Q000378:metabolism; D016923:Cell Death / Q000187:drug effects / Q000502:physiology; D004195:Disease Models, Animal; D004234:Diuretics, Osmotic / Q000494:pharmacology / Q000627:therapeutic use; D005609:Free Radicals / Q000037:antagonists & inhibitors / Q000378:metabolism; D005950:Glucose Solution, Hypertonic / Q000494:pharmacology* / Q000627:therapeutic use; D005979:Glutathione Peroxidase / Q000187:drug effects / Q000378:metabolism; D019586:Intracranial Hypertension / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology; D008315:Malondialdehyde / Q000378:metabolism; D008353:Mannitol / Q000494:pharmacology* / Q000627:therapeutic use; D009410:Nerve Degeneration / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology*; D010084:Oxidation-Reduction / Q000187:drug effects; D018384:Oxidative Stress / Q000187:drug effects / Q000502:physiology*; D051381:Rats
chemical_list: D000975:Antioxidants; D004234:Diuretics, Osmotic; D005609:Free Radicals; D005950:Glucose Solution, Hypertonic; D008353:Mannitol; D008315:Malondialdehyde; D002374:Catalase; D005979:Glutathione Peroxidase