Wefers H, Sies H
Institut für Physiologische Chemie I, Universität Düsseldorf, Federal Republic of Germany.
Eur J Biochem. 1988 Jun 1;174(2):353-7. doi: 10.1111/j.1432-1033.1988.tb14105.x.
Lipid peroxidation of rat liver microsomal fractions was monitored by its low-level chemiluminescence in preparations from controls and vitamin-E-deficient animals. Measurements were made (a) of the duration of the lag phase tau0 after initiation with NADPH/iron-ADP and (b) of the slope of the chemiluminescence increase. In microsomes with normal vitamin E (alpha-tocopherol) level the lag phase tau0 was substantially increased by ascorbate; in contrast, even an enhanced peroxidation was observed with ascorbate in vitamin-E-deficient microsomes. Therefore, the ascorbate-mediated protection of microsomal membranes against lipid peroxidation is dependent on vitamin E in the membrane. In vitamin E deficiency the pro-oxidant effect of ascorbate was abolished when glutathione (GSH) was present. Likewise, GSH does not prolong the lag phase tau0 in vitamin E deficiency. However, GSH (but not cysteine) exerts an antioxidant effect both in controls and in vitamin E deficiency by decreasing the slope of the chemiluminescence increase during lipid peroxidation. The involvement of GSH in an enzyme-dependent mechanism is suggested.
通过对照动物和维生素E缺乏动物制备物中的低水平化学发光监测大鼠肝微粒体部分的脂质过氧化。测量内容包括：(a) 用NADPH/铁-ADP引发后延迟期τ0的持续时间，以及 (b) 化学发光增加的斜率。在维生素E（α-生育酚）水平正常的微粒体中，抗坏血酸可显著延长延迟期τ0；相反，在维生素E缺乏的微粒体中，抗坏血酸甚至会导致过氧化增强。因此，抗坏血酸介导的微粒体膜对脂质过氧化的保护作用取决于膜中的维生素E。在维生素E缺乏时，当存在谷胱甘肽（GSH）时，抗坏血酸的促氧化作用被消除。同样，GSH在维生素E缺乏时也不会延长延迟期τ0。然而，GSH（而非半胱氨酸）通过降低脂质过氧化过程中化学发光增加的斜率，在对照和维生素E缺乏状态下均发挥抗氧化作用。提示GSH参与了一种酶依赖性机制。
