Protective effect of vitamin E on spinal cord injury by compression and concurrent lipid peroxidation

Iwasa, Kenichi; Ikata, Takaaki; Fukuzawa, Kenji

doi:10.1016/0891-5849(89)90067-1

Cited by 63 publications

(33 citation statements)

References 16 publications

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“…Further, the ROS level measured in the control-uninjured group in our study is comparable with that of healthy tissue of other e ective in vivo models. 20,21 Our measurements also indicate that our in vitro experimental condition was su cient to sustain the functional integrity of the extracted tissue. For example, electrophysiological recording, using double sucrose-gap chamber, showed that the isolated spinal cord tissue, when no deliberate compression was performed, was functionally competent by the end of the maximal experimental period (4 h) (Figure 2).…”

Section: Discussionmentioning

confidence: 59%

“…21 This demonstrates that the isolated spinal cord in our model retained the ability to produce signi®cant levels of ROS in the injured tissue. This elevation was produced in the absence of blood cells, such as neutrophils, which are considered to be a major source of free radicals 24 and responsible for subsequent cell damage 25 in in vivo studies.…”

Section: Discussionmentioning

confidence: 69%

“…20,21,32 For example, the LPO values range from about 6 ± 10 nmol/100 mg 20,21 to 158 nmol/100 mg 32 in the control. One possible explanation of such a phenomenon is the inability to standardize the experimental condition in these in vivo studies.…”

Section: Discussionmentioning

confidence: 94%

“…This level is also comparable with other in vivo studies. 20,21 Secondly, a standard compression produced an LPO level of 21.23+3.22 nmol/100 mg at 1 h after injury, a 200% increase from the control-uninjured group (P50.01, n=5). Thirdly, a treatment of either ascorbic acid or hypothermia to the compressed cords reduced the lipid peroxidation level of 17.96+3.0 nmol/100 mg and 16.43+2.89 nmol/100 mg; both are signi®cantly lower than those measured in the compression-untreated group (P50.01, n=5).…”

Section: Lipid Peroxidationmentioning

confidence: 93%

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The increase of reactive oxygen species and their inhibition in an isolated guinea pig spinal cord compression model

Luo

Robinson

et al. 2002

Spinal Cord

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Study design:In vitro studies using isolated guinea pig spinal cord. Objectives: To develop an alternative model using isolated guinea pig spinal cord, which can be used to screen antioxidants for in vivo SCI treatment. Setting: Department of Basic Medical Sciences, Purdue University, West Lafayette, Indiana, USA. Methods: The compression injury was induced by a constant-displacement of 5-s compression of spinal cord using a modi®ed forceps possessing a spacer. Reactive oxygen species (ROS) were evaluated using three distinct methods:¯uorescence microscopy, lipid peroxidation assay, and¯ow cytometry. Results: The injury-mediated ROS increases are comparable with other in vivo studies and consistent with our previous observation using a similar injury model and measured with electrophysiological and anatomical technique. Further, ascorbic acid, hypothermia, or the combination of both signi®cantly suppressed superoxide and lipid peroxidation. The combination treatment was the most e ective when compared with ascorbic acid or hypothermia alone. Conclusion: This in vitro model has the advantage of replicating some of the in vivo conditions while gaining the ability to control the experimental conditions. This in vitro model is suitable to study the mechanisms of ROS generation and degradation and can also be used to critically evaluate the e ective suppressor of ROS in the contents of spinal cord traumatic injury.

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Section: Discussionmentioning

confidence: 59%

Section: Discussionmentioning

confidence: 69%

Section: Discussionmentioning

confidence: 94%

Section: Lipid Peroxidationmentioning

confidence: 93%

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The increase of reactive oxygen species and their inhibition in an isolated guinea pig spinal cord compression model

Luo

Robinson

et al. 2002

Spinal Cord

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“…44,45 Iwasa et al 46 reported that LP is increased in an injured spinal cord and that dietary vitamin E e ectively protects the spinal cord from compression injury and subsequent LP in rats. Taoka et al 44 investigated the e ect of vitamin E on experimental compression injury of the spinal cord in vitamin E-de®cient rats.…”

Section: Discussionmentioning

confidence: 99%

Effect of methylprednisolone, tirilazad mesylate and vitamin E on lipid peroxidation after experimental spinal cord injury

et al. 1999

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E ect of methylprednisolone (MP), tirilazad mesylate (TM) and vitamin E on lipid peroxidation (LP) was evaluated in an experimental model of spinal cord compression injury in anesthetized rats. Forty rats, divided randomly into four groups, were injured by compressing on the spinal cord at Th 3 for 1 min. Bolus injections of saline solution, MP (30 mg/kg bolus and 5.4 mg/kg/h), TM (10 mg/kg four times per day), or vitamin E (30 mg/ kg four times per day) were begun 1 h after the spinal cord injury (SCI). Twenty-four hours after treatment, the rats were killed, and malondialdehyde (MDA), a LP product, was measured in the spinal cord tissues. Rats treated with MP, TM and vitamin E had signi®cantly decreased MDA levels (P50.01) than rats in the control group. The lowest MDA levels were found in the TM group. These results suggest that MP, TM and vitamin E may have a protective e ect against SCI in rats by its antioxidant e ect.

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Free Radicals and Acute Brain Injury: Mechanisms of Oxidative Stress and Therapeutic Potentials

Bayır

Kagan

2001

Brain Injury

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Protective effect of vitamin E on spinal cord injury by compression and concurrent lipid peroxidation

Cited by 63 publications

References 16 publications

The increase of reactive oxygen species and their inhibition in an isolated guinea pig spinal cord compression model

The increase of reactive oxygen species and their inhibition in an isolated guinea pig spinal cord compression model

Effect of methylprednisolone, tirilazad mesylate and vitamin E on lipid peroxidation after experimental spinal cord injury

Free Radicals and Acute Brain Injury: Mechanisms of Oxidative Stress and Therapeutic Potentials

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