Abstract

In the lumbar spinal cord of EAE guinea pigs a significant increase in SOD activity, lipid hydroperoxides content (more than 60%) and Fe2(+)-ascorbate-induced lipid peroxidation was observed. Multiple injections of cytochrome C-vitamin B2-vitamin PP (CV-combination) during the disease latent period resulted in suppression of EAE development. Supplementation with vitamin C, vitamin B12 or ATP eliminated this suppressive effect. Upon treatment with CV-combination beginning on the day of the first EAE clinical signs a half of the sick animals recovered. In their erythrocytes the ratio between SOD and catalase activities was normalized, though on a higher level. In the lumbar spinal cord the concentration of lipid hydroperoxides was decreased to the control one. Oxidative damage of the central nervous system is one of the mechanisms underlying the pathogenesis of lethal EAE.

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