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Anti‐oxidant capacity of spinal cord and erthrocytes of guinea pigs in case of experimental allergic encephalomyelitis and after disease suppression
Author(s) -
Kassabova T.,
Staykova M.,
Balevska P.,
Atanassov B.,
Goranov I.
Publication year - 1990
Publication title -
acta neurologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.967
H-Index - 95
eISSN - 1600-0404
pISSN - 0001-6314
DOI - 10.1111/j.1600-0404.1990.tb01599.x
Subject(s) - lipid peroxidation , spinal cord , encephalomyelitis , catalase , lumbar spinal cord , pathogenesis , vitamin , guinea pig , vitamin e , endocrinology , medicine , central nervous system , vitamin b12 , superoxide dismutase , immunology , oxidative stress , antioxidant , chemistry , biochemistry , psychiatry
In the lumbar spinal cord of EAE guinea pigs a significant increase in SOD activity, lipid hydroperoxides content (more than 60%) and Fe 2+ ‐ ascorbate‐induced lipid peroxidation was observed. Multiple injections of cytochrome C ‐ vitamin B 2 ‐ vitamin PP (CV‐combination) during the disease latent period resulted in suppression of EAE development. Supplementation with vitamin C, vitamin B 12 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.