Sagone A L, Wells R M, DeMocko C
Inflammation. 1980 Mar;4(1):65-71. doi: 10.1007/BF00914104.
Recent studies indicate that human granulocytes generate OH. during the phagocytosis of zymosan particles. Several theoretical considerations suggested to us that this OH. production might be related to prostaglandin metabolism, particularly the observation that OH. is generated by the reducation of hydroperoxides in microsomal systems. In our studies, we tested the importance of prostaglandin metabolism in the production of OH. by human granulocytes (PMNs). Indomethacin and aspirin at concentrations known to impair cyclooxygenase activity decreased OH. production by PMNs during the phagocytosis of zymosan particles. Phenol, which is known to alter prostaglandin metabolism, ablated OH. completely. None of these drugs at the concentrations used impaired the generation of O-2 or H2O2 by PMNs, as indicated by their failure to diminish significantly the generation of chemiluminescence. Thus, the decrement in OH. production by these drugs could not be attributed to a nonspecific effect on the production of O-2 or H2O2. These experiments therefore, indicate that the model for OH. production observed during prostaglandin synthesis with microsomal systems applies to human granulocytes.
最近的研究表明，人类粒细胞在吞噬酵母聚糖颗粒的过程中会产生羟基自由基（OH.）。一些理论上的思考使我们认为，这种羟基自由基的产生可能与前列腺素代谢有关，特别是基于在微粒体系统中通过过氧化氢的还原会产生羟基自由基这一观察结果。在我们的研究中，我们测试了前列腺素代谢在人类粒细胞（多形核白细胞，PMNs）产生羟基自由基过程中的重要性。已知会损害环氧化酶活性的吲哚美辛和阿司匹林浓度，会降低酵母聚糖颗粒吞噬过程中多形核白细胞产生羟基自由基的量。已知会改变前列腺素代谢的苯酚，会完全消除羟基自由基的产生。在所使用的浓度下，这些药物均未损害多形核白细胞产生超氧阴离子（O-2）或过氧化氢（H2O2），这一点从它们未能显著减少化学发光的产生可以看出。因此，这些药物导致羟基自由基产生量的减少不能归因于对超氧阴离子或过氧化氢产生的非特异性影响。因此，这些实验表明，在微粒体系统中前列腺素合成过程中观察到的羟基自由基产生模型适用于人类粒细胞。
