Karg E, Klivényi P, Németh I, Bencsik K, Pintér S, Vécsei L
Department of Pediatrics, Albert Szent-Györgyi University Medical School, Szeged, Hungary.
J Neurol. 1999 Jul;246(7):533-9. doi: 10.1007/s004150050399.
Free radical action has been suggested as a causal factor in multiple sclerosis. We investigated the plasma level of lipid peroxides expressed in terms of malone dialdehyde and changes in blood nonenzymatic antioxidants (glutathione, alpha-tocopherol, retinol, plasma sulfhydryl groups, and uric acid) in multiple sclerosis patients with exacerbation or in remission, including a group treated with beta-interferon. The malone dialdehyde level was increased by 38% (n.s.) during exacerbations. The blood concentration of oxidized glutathione was likewise elevated (P<0.05), while the ratio of plasma alpha-tocopherol to cholesterol plus triglyceride was decreased (P<0.001). These changes suggest increased free radical production and consumption of the scavenger molecules during the active phase of the disease. Blood reduced glutathione level was increased (P<0.01) during exacerbation and remission as well. The rise in this thiol is likely to be a compensatory mechanism defending the cells from further oxidant injuries. Beta-interferon increased plasma alpha-tocopherol levels (P<0.001) but not the lipid corrected alpha-tocopherol value. Other parameters were not influenced by the drug.
自由基作用被认为是多发性硬化症的一个致病因素。我们研究了以丙二醛表示的脂质过氧化物的血浆水平，以及多发性硬化症加重期或缓解期患者（包括一组接受β-干扰素治疗的患者）血液中非酶抗氧化剂（谷胱甘肽、α-生育酚、视黄醇、血浆巯基和尿酸）的变化。在病情加重期间，丙二醛水平升高了38%（无统计学意义）。氧化型谷胱甘肽的血浓度同样升高（P<0.05），而血浆α-生育酚与胆固醇加甘油三酯的比值降低（P<0.001）。这些变化表明在疾病的活动期自由基产生增加且清除分子被消耗。在病情加重期和缓解期，血液中还原型谷胱甘肽水平也升高（P<0.01）。这种硫醇的升高可能是一种保护细胞免受进一步氧化损伤的代偿机制。β-干扰素使血浆α-生育酚水平升高（P<0.001），但未使脂质校正的α-生育酚值升高。其他参数不受该药物影响。
