Shalabi E A
Department of Physiology, College of Medicine, King Saud University, Riyadh, Saudi Arabia.
Immunopharmacology. 1992 Jul-Aug;24(1):37-45. doi: 10.1016/0162-3109(92)90068-n.
The aim of the study is to investigate the effect of Acetaminophen (Am) on the oxidative respiratory burst of isolated human polymorphonuclear leukocytes (PMNs). Acetaminophen inhibited the luminolchemiluminescence (CL) peak response of PMNs stimulated with phorbol myristate acetate (PMA) or opsonized zymosan in a concentration dependent manner. The inhibitory effect of Am on PMA-stimulated PMNs-CL response was partially reversible. The level of CL inhibition with Am plus the hydroxyl radical scavengers allopurinol, dimethyl sulfoxide (DMSO) or superoxide dismutase (SOD) is greater than that with Am alone. Generation of superoxide (O2-) by stimulated PMNs, as assayed by superoxide dismutase inhibitable reduction of Ferricytochrome c, was markedly inhibited by Am. Furthermore, the phagocytic activity of PMNs as tested for by the ingestion of opsonized dead yeast was significantly reduced in Am-treated cells. These results indicate clearly that Am causes significant inhibition of the human PMNs function in vitro.
本研究的目的是调查对乙酰氨基酚(Am)对分离的人多形核白细胞(PMN)氧化呼吸爆发的影响。对乙酰氨基酚以浓度依赖性方式抑制佛波酯(PMA)或调理酵母聚糖刺激的PMN的鲁米诺化学发光(CL)峰值反应。Am对PMA刺激的PMN-CL反应的抑制作用部分可逆。Am与羟基自由基清除剂别嘌呤醇、二甲基亚砜(DMSO)或超氧化物歧化酶(SOD)联合使用时的CL抑制水平高于单独使用Am时。通过超氧化物歧化酶可抑制的铁细胞色素c还原测定,刺激的PMN产生超氧化物(O2-)被Am显著抑制。此外,在经Am处理的细胞中,通过吞噬调理的死酵母测试的PMN吞噬活性显著降低。这些结果清楚地表明,Am在体外对人PMN功能有显著抑制作用。