Hoffeld J T
Eur J Immunol. 1981 May;11(5):371-6. doi: 10.1002/eji.1830110505.
A broad spectrum of agents known to block various steps in the lipid peroxidation process were tested for their ability to protect mouse spleen cells and thereby enhance their activities, in vitro, in either the primary antibody response or the lipopolysaccharide-stimulated proliferation response. Each agent (superoxide dismutase, butylated hydroxyanisole/butylated hydroxytoluene/n-propyl gallate, lucigenin, and alpha-tocopherol) was able to enhance the cellular response in both assay systems. The degree of enhancement of these immune functions was in proportion to the efficacy of each agent in blocking the overall process in lipid peroxidation. Previous work in this laboratory has shown that the enhancement of the primary antibody response by 2-mercaptoethanol (2-ME) is mediated by the enhanced availability of reduced glutathione in the culture medium. Suboptimal doses of each lipid antioxidant agent were able to enhance the antibody response in the additive manner with a suboptimal dose of 2-ME up to a maximum response equal to that achieved with an optimal dose of 2-ME alone. These data support the hypothesis that the enhancement of cellular responses in the presence of 2-ME is mediated by the lipid antioxidant activity of reduced glutathione.
测试了一系列已知可阻断脂质过氧化过程中各个步骤的试剂,以考察它们在体外保护小鼠脾细胞并增强其活性的能力,这些活性涉及初次抗体反应或脂多糖刺激的增殖反应。每种试剂(超氧化物歧化酶、丁基羟基茴香醚/丁基化羟基甲苯/没食子酸正丙酯、光泽精和α-生育酚)在两种检测系统中均能增强细胞反应。这些免疫功能的增强程度与每种试剂阻断脂质过氧化总体过程的功效成正比。本实验室先前的研究表明,2-巯基乙醇(2-ME)增强初次抗体反应是由培养基中还原型谷胱甘肽可用性的提高介导的。每种脂质抗氧化剂的次优剂量能够与次优剂量的2-ME以相加的方式增强抗体反应,直至达到与单独使用最佳剂量的2-ME所实现的最大反应相同的程度。这些数据支持以下假设:在2-ME存在的情况下细胞反应的增强是由还原型谷胱甘肽的脂质抗氧化活性介导的。