Lipid peroxidation in experimental spinal cord injury: time-level relationship

Barut, Şeref; Canbolat, Ali; Bılge, Turgay; Aydın, Yunus; Çokneşeli, Baki; Kaya, Umur

doi:10.1007/bf00308614

Cited by 77 publications

(47 citation statements)

References 46 publications

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“…4,5 The extent of lipid peroxidation is a useful parameter for evaluating cellular disturbances caused by spinal cord trauma under experimental conditions. [32][33][34] The literature mentioned above outlines the biochemical basis and evidence for the occurrence of oxygen radical generation and lipid peroxidation during the acute phase of central nervous system (CNS) trauma or stroke (ischemic and hemorrhagic).…”

Section: Discussionmentioning

confidence: 99%

Protective effect of melatonin on experimental spinal cord ischemia

et al. 2003

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Study design: Experimental animal model to assess ischemic spinal cord injury following occlusion of the thoraco-abdominal aorta. Objectives: To measure whether melatonin administered to rabbits before and after occlusion exerts an effect on the repair of ischemia-reperfusion (IR) injury. Setting: Medical Biology Laboratory, Inonu University, Malatya, Turkey Methods: Rabbits were divided into three IR treatment groups and one sham-operated (ShOp) control group. The three treatment groups had their infrarenal aorta temporarily occluded for 25 min, while the ShOp group had laparotomy without aortic occlusion. Melatonin was administered either 10 min before aortic occlusion or 10 min after the clamp was removed. Physiologic saline was administered to the control animals. After treatment, the animals were euthanized and lumbosacral spinal cord tissue was removed for the determination of relevant enzyme activities. Results: Malondialdehyde levels, indicating the extent of lipid peroxidation, were found to be significantly increased in the nonmelatonin treated (IR) group when compared to the ShOp group. Melatonin, whether given to pre-or post occlusion groups, suppressed malondialdehyde levels below that of the ShOp group. Catalase (CAT) and glutathione peroxidase (GSH-Px) enzyme activities were increased in the IR group compared to the ShOp group. Melatonin given preocclusion resulted in a significant decrease in both CAT and GSH-Px enzyme levels. The superoxide dismutase (SOD) enzyme activity was decreased in the ischemia-reperfusion treatment group. However, the melatonin treatment increased SOD enzyme activity to levels approximating that of the ShOp group. Conclusion: To our knowledge, this is the first study that shows the effects of melatonin administered both pre-and postischemia on induced oxidative damage to injured spinal cords. Our data also expands on reports that melatonin administration may significantly reduce the incidence of spinal cord injury following temporary aortic occlusion.

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Section: Discussionmentioning

confidence: 99%

Protective effect of melatonin on experimental spinal cord ischemia

et al. 2003

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“…36,39 ± 42 It was shown that lipid peroxidation levels reached its maximum at 1 h after experimental spinal cord injury. 39 Therefore, we have started the cooling procedure 30 min after the injury and continued for 30 min. Perfusion of the injured or ischemic spinal cord with a cool, isotonic solution has been used in animal models 1,3,6 and humans and has shown some promise.…”

Section: Discussionmentioning

confidence: 99%

The effect of epidural cooling on lipid peroxidation after experimental spinal cord injury

et al. 1998

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Study Design: The e ect of epidural space perfusion with chilled saline solution (% 0.9 NaCl) on lipid peroxidation after experimental spinal cord injury in rats was evaluated. Objectives: The extent of lipid peroxidation is a useful parameter for evaluating the cellular disturbance caused by spinal cord trauma in experimental conditions. The protective e ects of hypothermia against neurological injury resulting from trauma or ischemia both in experimental and clinical situations have been demonstrated. Setting: Departments of Neurosurgery and Biochemistry, Cerrahpasa Medical School, Istanbul, Turkey. Methods: Twenty-®ve female Wistar Albino rats were used. There were ®ve rats in group I (sham-operated), seven rats in group II (trauma), and eight rats in group III (epidural cooling). The remaining ®ve rats were used for the pilot study to determine the spinal cord and body temperature. A clip compression method was used to produce acute spinal cord injury. In group III, 30 min after the trauma the injured spinal cord was cooled by perfusion of the epidural space with chilled saline solution (% 0.9 NaCl) with a¯ow rate of 5 ml/min for 30 min. At 2 h after trauma, all rats other than the ones used in the pilot study, were sacri®ced and the spinal cords were excised. The extent of lipid peroxidation in the spinal cord was assessed by measuring the tissue content of malonil dialdehyde (MDA). Results: The tissue MDA contents were 1.58 micromol MDA/gram wet weight (gww) in group 1 (sham-operated), 2.58 micromol MDA/gww in group 2 (trauma), and 1.77 micromol/ gww in group 3 (epidural cooling), the di erences being statistically signi®cant. Conclusion:The results indicated that epidural cooling of traumatized spinal cord is e ective in preventing secondary damage due to the peroxidation of lipid membranes.

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“…Increased levels of MDA were also seen in the contused rat spinal cord as early as 30 minutes post-SCI, which peaked at 3 h and returned to baseline by 12 h [26]. In a compression SCI model, MDA was significantly increased by 15 minutes, peaked at 1 h and then fell thereafter [122], suggesting that there is not much difference between the cat contusion and rat compression models at least as far as the onset of post-SCI LP. However, two unfortunate limitations of these studies were the choice of MDA, which is a biomarker of enzymatic LP during the arachidonic acid cascade, as well as free radical-induced LP, and the fact that postinjury times longer than 12 h were not included.…”

Section: Onset and Duration Of Oxidative Damage In The Injured Spinalmentioning

confidence: 99%

Antioxidant Therapies for Acute Spinal Cord Injury

2011

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Summary:One of the most investigated molecular mechanisms involved in the secondary pathophysiology of acute spinal cord injury (SCI) is free radical-induced, iron-catalyzed lipid peroxidation (LP) and protein oxidative/nitrative damage to spinal neurons, glia, and microvascular cells. The reactive nitrogen species peroxynitrite and its highly reactive free radicals are key initiators of LP and protein nitration in the injured spinal cord, the biochemistry, and pathophysiology of which are first of all reviewed in this article. This is followed by a presentation of the antioxidant mechanistic approaches and pharmacological compounds that have been shown to have neuroprotective properties in preclinical SCI models. Two of these, which act by inhibition of LP, are high-dose treatment with the glucocorticoid steroid methylprednisolone (MP) and the nonglucocorticoid 21-aminosteroid tirilazad, have been demonstrated in the multicenter NASCIS clinical trials to produce at least a modest improvement in neurological recovery when administered within the first 8 hours after SCI. Although these results have provided considerable validation of oxidative damage as a clinically practical neuroprotective target, there is a need for the discovery of safer and more effective antioxidant compounds for acute SCI.

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Lipid peroxidation in experimental spinal cord injury: time-level relationship

Cited by 77 publications

References 46 publications

Protective effect of melatonin on experimental spinal cord ischemia

Protective effect of melatonin on experimental spinal cord ischemia

The effect of epidural cooling on lipid peroxidation after experimental spinal cord injury

Antioxidant Therapies for Acute Spinal Cord Injury

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