Brett R, Rumsby M G
Department of Biology, University of York, England.
Neurochem Int. 1993 Jul;23(1):35-44. doi: 10.1016/0197-0186(93)90141-q.
Central nervous system tissue from guinea-pigs in various stages of chronic relapsing experimental allergic encephalomyelitis (CR-EAE) has been analysed for evidence of free radical damage using the thiobarbituric acid test as an indicator of oxidative changes. Levels of thiobarbituric acid-reactive materials in brain and spinal cord regions from prolonged acute and early relapse phases of CR-EAE were significantly higher than in central nervous system tissue from Freund's adjuvant control and normal uninoculated animals. In the late relapse phase of CR-EAE, levels of thiobarbituric acid-reactive materials in CNS samples were at control values. Fluorescence analysis of central nervous system tissue confirmed evidence of increased free radical damage in prolonged acute and early relapse stages of CR-EAE. The increased oxidative damage observed in the central nervous system in CR-EAE is discussed in relation to the role of macrophages and their oxidative burst.
利用硫代巴比妥酸试验作为氧化变化的指标,对处于慢性复发性实验性变应性脑脊髓炎(CR-EAE)不同阶段的豚鼠中枢神经系统组织进行了自由基损伤证据分析。CR-EAE的长期急性期和早期复发期脑和脊髓区域中硫代巴比妥酸反应性物质的水平显著高于弗氏佐剂对照组和未接种的正常动物的中枢神经系统组织。在CR-EAE的晚期复发期,中枢神经系统样本中硫代巴比妥酸反应性物质的水平处于对照值。中枢神经系统组织的荧光分析证实了CR-EAE长期急性期和早期复发期自由基损伤增加的证据。结合巨噬细胞的作用及其氧化爆发,讨论了在CR-EAE中枢神经系统中观察到的氧化损伤增加的情况。