Gutin P H, Levin K J, McDermott M W, Hooper N, Smith M T, Cashman J R, Chan P H, Ross G Y, Phillips T L, Levin V A
Department of Neurological Surgery, School of Medicine, University of California, San Francisco.
Int J Radiat Oncol Biol Phys. 1993 Jan;25(1):67-72. doi: 10.1016/0360-3016(93)90146-m.
We tested the role of lipid peroxidation in the demyelination and white matter necrosis associated with radiation injury of the central nervous system.
We irradiated the cervical spinal cords of female F344 rats (23 Gy) and assayed for the accumulation of the peroxidation byproducts malondialdehyde and hydroxyeicosatetraenoic acids, and for the consumption of the endogenous free radical scavengers vitamins E and C. We further tested the role of lipid peroxidation in radiation injury of the central nervous system by determining the sensitivity of the cervical spinal cord to radiation in rats on diets containing deficient, normal, and supplemental levels of the antioxidant vitamin E. Rats were placed on these diets at 4 weeks of age and irradiated (18.5-21.5 Gy) 16 weeks later.
During the 5 months between irradiation and the onset of paralysis, no accumulation of peroxidation byproducts or consumption of endogenous scavengers was seen in the cervical spinal cords of the irradiated rats. The cervical spinal cords of some of the rats placed on the diets with deficient, normal, and supplemental levels of vitamin E were analyzed at the time of irradiation and contained 197 +/- 57, 501 +/- 19, and 717 +/- 35 pmol vitamin E/mg protein, respectively. Despite the statistical differences in these levels, the radiation sensitivity of the cervical spinal cord (ED50 for white matter necrosis) in rats receiving the three diets was not different (20.4, 20.7, and 20.6 Gy).
These data do not support a role for free radical-induced lipid peroxidation in the white matter damage seen in radiation injury of the central nervous system.
我们测试了脂质过氧化在与中枢神经系统辐射损伤相关的脱髓鞘和白质坏死中的作用。
我们对雌性F344大鼠的颈脊髓进行照射（23 Gy），并检测过氧化副产物丙二醛和羟基二十碳四烯酸的积累情况，以及内源性自由基清除剂维生素E和维生素C的消耗情况。我们还通过测定食用含有缺乏、正常和补充水平抗氧化剂维生素E饮食的大鼠颈脊髓对辐射的敏感性，进一步测试了脂质过氧化在中枢神经系统辐射损伤中的作用。大鼠在4周龄时开始食用这些饮食，并在16周后进行照射（18.5 - 21.5 Gy）。
在照射至瘫痪发作的5个月期间，未在受照射大鼠的颈脊髓中观察到过氧化副产物的积累或内源性清除剂的消耗。在照射时，对一些食用缺乏、正常和补充水平维生素E饮食的大鼠的颈脊髓进行分析，其维生素E含量分别为197±57、501±19和717±35 pmol维生素E/毫克蛋白质。尽管这些水平存在统计学差异，但接受三种饮食的大鼠颈脊髓的辐射敏感性（白质坏死的半数有效剂量）并无差异（分别为20.4、20.7和20.6 Gy）。
这些数据不支持自由基诱导的脂质过氧化在中枢神经系统辐射损伤所见的白质损伤中起作用。
