Lemke M, Frei B, Ames B N, Faden A I
Department of Neurology, University of California San Francisco.
Neurosci Lett. 1990 Jan 1;108(1-2):201-6. doi: 10.1016/0304-3940(90)90731-n.
Generation of free radicals and subsequent lipid peroxidation have been proposed to contribute to delayed tissue damage following traumatic spinal cord injury (SCI). Ubiquinols (reduced coenzyme Q), ascorbate (vitamin C), and alpha-tocopherol (vitamin E) are endogenous antioxidants; decreases in tissue levels of these compounds may, therefore, reflect ongoing oxidative reactions. In the present studies, alterations in tissue levels of ubiquinol-9 and -10, ascorbate, and alpha-tocopherol were examined after SCI of varying severity in the rat. Levels of alpha-tocopherol did not change significantly after injury. Ascorbate and ubiquinol levels were decreased after trauma. Changes in tissue levels of ubiquinol, but not ascorbate reflected the degree of trauma. Thus, ubiquinol levels may provide a useful marker of the oxidative component of the secondary injury response.
自由基的产生及随后的脂质过氧化作用被认为与创伤性脊髓损伤（SCI）后延迟性组织损伤有关。泛醇（还原型辅酶Q）、抗坏血酸（维生素C）和α-生育酚（维生素E）是内源性抗氧化剂；因此，这些化合物组织水平的降低可能反映了正在进行的氧化反应。在本研究中，检测了大鼠不同严重程度脊髓损伤后泛醇-9和-10、抗坏血酸以及α-生育酚的组织水平变化。损伤后α-生育酚水平无显著变化。创伤后抗坏血酸和泛醇水平降低。泛醇组织水平的变化而非抗坏血酸的变化反映了创伤程度。因此，泛醇水平可能为继发性损伤反应的氧化成分提供一个有用的标志物。
