Dri P, Berton G, Patriarca P
Inflammation. 1981 Sep;5(3):223-39. doi: 10.1007/BF00914446.
The protease inhibitor, L-1-tosylamide-2-phenylethylchloromethyl ketone (TPCK), stimulated the O2- production, H2O2 generation, oxygen consumption, and the hexose monophosphate shunt of guinea pig peritoneal polymorphs. Other protease inhibitors were not able to stimulate the metabolic burst of these cells. Maximum stimulation was obtained at 100 microM concentration of the compound. No stimulation was seen in human blood polymorphs even at concentrations higher than those effective on guinea pig polymorphs. TPCK also stimulated the oxidative metabolism of guinea pig blood polymorphs and of guinea pig resident peritoneal macrophages. At concentrations which did not stimulate the oxidative metabolism of guinea pig polymorphs, TPCK inhibited the O2- production induced in these cells by treatment with phorbol myristate acetate (PMA) or with other soluble stimuli. Other protease inhibitors also inhibited the respiratory burst induced by PMA. It is concluded that TPCK exerts two effects on the metabolism of guinea pig phagocytes, which are probably mediated by different mechanisms. The inhibitory effect on the PMA-stimulated respiratory burst might be related to the antiprotease activity of TPCK, while the stimulation of the respiratory burst seems to be independent of protease inhibition.
蛋白酶抑制剂L-1-甲苯磺酰氨基-2-苯乙基氯甲基酮（TPCK）可刺激豚鼠腹腔多形核白细胞产生超氧阴离子（O₂⁻）、生成过氧化氢（H₂O₂）、消耗氧气以及促进磷酸己糖旁路代谢。其他蛋白酶抑制剂无法刺激这些细胞的代谢爆发。该化合物在100微摩尔浓度时可获得最大刺激效果。即使在高于对豚鼠多形核白细胞有效浓度的情况下，人血多形核白细胞也未见刺激反应。TPCK还可刺激豚鼠血液多形核白细胞和豚鼠驻留腹腔巨噬细胞的氧化代谢。在未刺激豚鼠多形核白细胞氧化代谢的浓度下，TPCK可抑制用佛波酯（PMA）或其他可溶性刺激物处理这些细胞所诱导的O₂⁻产生。其他蛋白酶抑制剂也可抑制PMA诱导的呼吸爆发。结论是，TPCK对豚鼠吞噬细胞的代谢有两种作用，可能由不同机制介导。对PMA刺激的呼吸爆发的抑制作用可能与TPCK的抗蛋白酶活性有关，而对呼吸爆发的刺激作用似乎与蛋白酶抑制无关。
