Shalabi E A, al-Tuwaijri A S
Department of Physiology, College of Medicine, King Saud University, Riyadh, Saudi Arabia.
Biopharm Drug Dispos. 1996 Aug;17(6):501-9. doi: 10.1002/(SICI)1099-081X(199608)17:6<501::AID-BDD968>3.0.CO;2-1.
The effect of high temperatures (39, 41, and 43 degrees C) on acetaminophen (AM-) induced inhibition of the oxidative respiratory burst of polymorphonuclear leukocytes (PMNs) in vitro has been examined. Whole blood or isolated human PMNs were exposed to various temperatures in vitro in the presence or absence of AM for 0-90 min. Phagocyte membrane-bound NADPH oxidase was studied using the luminol chemiluminescence (CL) response and the superoxide dismutase inhibitable reduction of ferricytochrome C. The NADPH oxidase was stimulated by phorbol myristate acetate (PMA). The results showed that high temperatures (39-43 degrees C) potentiate the AM inhibitory effect on CL peak response of phagocytes in a temperature-dependent manner. Furthermore, the inhibition of superoxide (O2-) production induced by AM was potentiated by incubating the cells at 39 or 43 degrees C at different time intervals. These studies suggest that high temperatures significantly potentiate the AM inhibitory effect on oxidative metabolism of PMNs in vitro. These actions of AM may influence the outcome in patients with infectious febrile conditions.
研究了高温（39、41和43摄氏度）对乙酰氨基酚（AM）在体外诱导的多形核白细胞（PMN）氧化呼吸爆发抑制作用的影响。全血或分离的人PMN在有或无AM的情况下于体外暴露于不同温度0至90分钟。使用鲁米诺化学发光（CL）反应和超氧化物歧化酶可抑制的细胞色素C还原研究吞噬细胞膜结合的NADPH氧化酶。NADPH氧化酶由佛波酯（PMA）刺激。结果表明，高温（39 - 43摄氏度）以温度依赖性方式增强AM对吞噬细胞CL峰值反应的抑制作用。此外，通过在39或43摄氏度下以不同时间间隔孵育细胞，AM诱导的超氧化物（O2-）产生的抑制作用增强。这些研究表明，高温显著增强AM在体外对PMN氧化代谢的抑制作用。AM的这些作用可能会影响感染性发热疾病患者的病情转归。
