Activity of mannitol and hypertonic saline therapy on the oxidant and antioxidant system during the acute term after traumatic brain injury in the rats.
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.
Yilmaz
Nebi
N
Department of Neurosurgery, School of Medicine, Yuzuncu Yil University, Van, Turkey. yilmaznebi@yahoo.com
Dulger
Haluk
H
Kiymaz
Nejmi
N
Yilmaz
Cahide
C
Gudu
Burhan O
BO
Demir
Ismail
I
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
D000975:Antioxidants; D004234:Diuretics, Osmotic; D005609:Free Radicals; D005950:Glucose Solution, Hypertonic; D008353:Mannitol; D008315:Malondialdehyde; D002374:Catalase; D005979:Glutathione Peroxidase