Superoxide radicals play important roles in the pathogenesis of spinal cord injury

Taoka, Yuji; Naruo, Masakuni; Koyanagi, Eiichi; Urakado, Misao; Inoue, Masayasu

doi:10.1038/sc.1995.98

Cited by 38 publications

(24 citation statements)

References 19 publications

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“…15 However, Nishibe showed that SOD activity is generally much lower than that of CAT activity in spinal cord tissues. 40 Therefore, SOD activity changes observed due to melatonin treatment are less pronounced than those seen in CAT.…”

Section: Discussionmentioning

confidence: 99%

“…11,18,[26][27][28][29][30] Free oxygen radicals can impair the function of the cellular components. 14,15,31 Free oxygen radical-induced damage has been implemented in postischemic cell injury and cell death, while free radical scavengers such as SOD, CAT and GSH-Px are associated with partial amelioration of ischemic injury. 4,5 The extent of lipid peroxidation is a useful parameter for evaluating cellular disturbances caused by spinal cord trauma under experimental conditions.…”

Section: Discussionmentioning

confidence: 99%

“…Among these, the enzymes superoxide dismutase (SOD, EC 1.15.1.1), catalase (CAT, EC 1.11.1.6), and glutathione peroxidase (GSH-Px, EC 1.11.1.9) are the best-known components of the biological protective system. [12][13][14][15] It is recognized that these enzymes may be important protectors against lipid peroxidation and damage due to free radicals after the onset of neuronal ischemia.…”

Section: Introductionmentioning

confidence: 99%

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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%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Protective effect of melatonin on experimental spinal cord ischemia

et al. 2003

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“…[5][6][7] Previous studies have demonstrated that the formation of ROS including hydroxyl radical, superoxide and hydrogen peroxide immediately after central nervous system injury may contribute to the pathogenesis of SCI. 8,9 Source of ROS. Production of ROS under physiological conditions is important for normal cellular redox reactions.…”

Section: Ros and Oxidative Stress In Scimentioning

confidence: 99%

Oxidative stress in spinal cord injury and antioxidant-based intervention

Jia

Zhu

Li³

et al. 2011

Spinal Cord

259

176

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Study design: Literature review. Objectives: Spinal cord injury (SCI) remains a major public health issue in developed countries as well as worldwide. The pathophysiology of SCI is characterized by an initial primary injury followed by secondary deterioration. Although the etiology and pathogenesis of SCI remain to be fully understood, it has been suggested that reactive oxygen species (ROS) and oxidative stress have a significant role in the pathophysiology of SCI. Thus, alleviating oxidative stress may be an effective strategy for therapeutic intervention of SCI. The aim of this review was to describe (i) the sources of ROS as well as the major antioxidant defenses with particular attention being paid to lipid peroxidation; (ii) the biomarkers of oxidative stress in SCI and (iii) the neuroprotective effects of various compounds with antioxidative properties in animal models of SCI. Methods: PubMed, one of the most comprehensive biomedical databases, was searched from 1976-2011. All relevant papers were read by title, abstract and full-length article. Results: Oxidative stress is considered a hallmark of injury of SCI. Thus, alleviating oxidative stress may be an effective way of therapeutic intervention of SCI. Two of these agents, the glucocorticoid steroid methylprednisolone and the non-glucocorticoid 21-aminosteroid tirilazad, have been shown to possess significant antioxidant activities and improve recovery of SCI patients in clinical trials. Other promising botanical compounds and their molecular targets and mechanisms of action with regard to potential protection against SCI were also described. These include carotenoids and phenolic compounds. Conclusion: ROS and oxidative stress have a significant role in the pathophysiology of SCI. Alleviating oxidative stress is be an effective strategy for therapeutic intervention of SCI. Extensive research over the past several decades has identified numerous bioactive compounds that have antioxidative stress benefits in animal models of SCI. Thus, continued studies on bioactive compounds with ROS-scavenging capacity may lead to the development of effective antioxidant-based modalities for treating SCI in human subjects.

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“…NRF2 promotes neuronal survival in neurodegeneration and acute nerve damage been observed in such conditions, and thus antioxidation strategies may prove beneficial for these cases as well (33)(34)(35). Whereas photoreceptor cells are highly specialized and unusual neurons, retinal ganglion cells (RGCs) are more typical of the types of CNS projection neurons that suffer damage in acute crush injuries.…”

Section: Introductionmentioning

confidence: 99%