Conkling P, Cornwell D G, Sagone A L
Inflammation. 1985 Jun;9(2):149-61. doi: 10.1007/BF00917587.
Recent evidence indicates that phagocytic cells play a major role in tissue inflammation. The release of enzymes, lipid metabolites such as prostaglandins, and reactive oxygen species by these cells appear to mediate the inflammatory process. In this study we have evaluated the effects of diethyldithiocarbamate (DDC) on human monocyte function and metabolism. We demonstrate that DDC impairs that antibody-dependent cytoxicity (ADCC) of monocytes to red cell targets. The concentration of DDC which caused maximal suppression of ADCC also prevented the burst of oxidative metabolism in monocytes stimulated by sensitized red cells targets or phorbol myristate acetate (PMA). DDC also impairs the lipid metabolism of these cells as indicated by a decrement in malonyldialdehyde (MDA) production. These data indicate that DDC impairs the activity of two major biochemical pathways in monocytes which are related to the inflammatory process, i.e., the release of oxygen metabolites and prostaglandins.
近期证据表明,吞噬细胞在组织炎症中起主要作用。这些细胞释放的酶、脂质代谢产物(如前列腺素)和活性氧似乎介导了炎症过程。在本研究中,我们评估了二乙基二硫代氨基甲酸盐(DDC)对人单核细胞功能和代谢的影响。我们证明,DDC损害单核细胞对红细胞靶标的抗体依赖性细胞毒性(ADCC)。导致ADCC最大抑制的DDC浓度也阻止了由致敏红细胞靶标或佛波酯(PMA)刺激的单核细胞氧化代谢爆发。DDC还损害这些细胞的脂质代谢,表现为丙二醛(MDA)生成减少。这些数据表明,DDC损害了单核细胞中与炎症过程相关的两条主要生化途径的活性,即氧代谢产物和前列腺素的释放。