Fülöp T, Varga Z, Nagy J T, Fóris G
First Department of Medicine, Medical University of Debrecen, Hungary.
Biochem Int. 1988 Sep;17(3):419-26.
The O2- production as a marker of the respiratory burst was investigated under various stimulations in polymorphonuclear leukocytes of healthy young and aged subjects. Stimulation of the respiratory burst in the cells of elderly by specific agents (opsonized zymozan, N-formyl-methionyl-leucyl-phenylalanine, carbachol) resulted in a diminished response while it remained unchanged on the effect of non-specific stimulation (A23187, phorbol myristate acetate) comparing to young subjects. To elucidate the postreceptor signal transduction mechanism involved in respiratory burst stimulation various inhibitors were used as follows: neomycin (for phospholipase C enzyme), mepacrine (for phospholipase A2 enzyme) and pertussis toxin (for GTP binding regulatory protein). The results suggest that phospholipase C as well as phospholipase A2 could be involved in the postreceptor signal transduction depending on the stimulus, but the impairment of the pertussis toxin sensitive GTP binding protein with aging might explain the decrease response of the respiratory burst after stimulating the different receptors.
在健康年轻和老年受试者的多形核白细胞中,研究了作为呼吸爆发标志物的超氧阴离子(O2-)产生情况,观察其在各种刺激下的变化。与年轻受试者相比,特定试剂(调理酵母聚糖、N-甲酰甲硫氨酰亮氨酰苯丙氨酸、卡巴胆碱)刺激老年受试者细胞的呼吸爆发时,反应减弱,而非特异性刺激(A23187、佛波酯)的效果则无变化。为阐明参与呼吸爆发刺激的受体后信号转导机制,使用了以下各种抑制剂:新霉素(针对磷脂酶C酶)、米帕林(针对磷脂酶A2酶)和百日咳毒素(针对GTP结合调节蛋白)。结果表明,磷脂酶C以及磷脂酶A2可能根据刺激的不同参与受体后信号转导,但随着年龄增长,百日咳毒素敏感的GTP结合蛋白受损可能解释了刺激不同受体后呼吸爆发反应降低的原因。