Effect of Methylprednisolone on Cytochrome Oxidase and Lipid Peroxidation of the Contused Spinal Cord.
- Author:
Kyu Man SHIN
1
;
Sung Hak KIM
Author Information
1. Department of Neurosurgery, College of Medicine, Ewha Womans University, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Cytochrome oxidase;
Lipid peroxidation;
Methylprednisolone;
Spinal cord injury
- MeSH:
Animals;
Cats;
Contusions;
Cytochromes*;
Electron Transport Complex IV*;
Lipid Peroxidation*;
Methylprednisolone Hemisuccinate;
Methylprednisolone*;
Mitochondria;
Spinal Cord Injuries;
Spinal Cord*
- From:Journal of Korean Neurosurgical Society
1984;13(4):635-643
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
The purpose of this study was to determine the beneficial effect of treatment with methylprednisolone sodium succinate on the cytochrome oxidase activity and lipid peroxidation during 4 hour after 400gm-cm injury to the cat spinal cord. The contusion injury was associated with a decrease of the cytochrome oxidase activity of the gray matter and an increase of the lipid peroxidation. A significant drop in cytochrome oxidase activity to about 40% of normal level was observed as early as 15 minutes after injury and the lowest activity was reached at 1 hour postinjury, but at 4 hours after injury the level of the activities of the enzyme was increased or stabilized. An increase of lipid peroxidation began as early as 15 minutes after the injury and the highest concentration was reached at 4 hour of postinjury. An intravenous dose of 30mg/kg methylprednisolone sodium succinate was administered immediately after the injury. The significant increased of the cytochrome oxidase activity and concomitant decrease of the lipid peroxidation were found in cats of the treated methylprednislone. These results suggest that the beneficial effects of 30mg/kg dose administration of the methylprednisolone are an enhancement of cytochrome oxidase activity, ie., the mitochondria function and an attenuation of lipid peroxide formation, as the result of the inhibition of the O2-free radial reaction.
