The effects of chronic alpha-tocopherol administration on lipid peroxidation in an experimental model of acute spinal cord injury.
Most of the numerous experimental studies to research pathophysiological changes following acute spinal cord injury suggest a two-step mechanism of damage to the spinal cord in which the primary (direct) or mechanical injury caused by the trauma initiates secondary (indirect) or progressive autodestructive injury of the cord. During recent years, free oxygen radical generation and lipid peroxidation have been considered to be responsible for secondary autodestructive injury. Alpha tocopherol occupies an important and unique position in the overall antioxidant defense. Alpha tocopherol-depleted animals are generally more susceptible to the adverse effects of environmental agents than are supplemented animals. This study was planned to study the effectiveness in counteracting this autodestructive process by supplementing alpha-tocopherol in rats maintained on a nutritionally adequate diet, and also to evaluate whether it will provide additional protection or not. Eighty healthy Wistar rats (treatment and controls) were included. The treatment group received 100 mg/kg alpha tocopherol each day, intraperitoneally for seven days. Using a standard acute spinal cord trauma model in Wistar rats trauma was applied, an malondialdehyde (MDA) which is a lipid peroxidation product was measured in the traumatized spinal cord at various times following the trauma in order to indirectly evaluate the lipid peroxidation and generation of free oxygen radicals in a time sequence. Statistical analysis of the values demonstrated that malondialdehyde formation in the alpha-tocopherol administered group was significantly lower than in the control group. These findings indicate that longterm administration of alpha-tocopherol may be useful to decrease lipid peroxidation following acute spinal cord trauma.
Bozbuğa
M
M
Department of Neurosurgery, Kartal Research and Teaching Hospital, Istanbul, Turkey.
Izgi
N
N
Canbolat
A
A
D000818:Animals; D005260:Female; D005609:Free Radicals / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects*; D008315:Malondialdehyde / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013119:Spinal Cord Injuries / Q000378:metabolism*; D014810:Vitamin E / Q000494:pharmacology*
D005609:Free Radicals; D014810:Vitamin E; D008315:Malondialdehyde