Maubach K, Foey A D, Hall N D
Bath Institute for Rheumatic Diseases, University of Bath, UK.
Agents Actions. 1993;39 Spec No:C107-9. doi: 10.1007/BF01972737.
Ion-motive ATPase play an essential role in many aspects of cell biology, including mononuclear cell (MNC) functions relevant to chronic inflammation. For example, ouabain, a specific inhibitor of Na+, K+ ATPase, suppresses both T and B cell proliferation but induces synthesis of IL-1. Using a cytochemical assay quantified by microdensitometry, total and ouabain-sensitive ATPase activities have been compared in MNC from rheumatoid and control subjects. The sensitivity of these enzymes to inactivation by thiol-blocking reagents has been studied by preincubation with an impermeant SH blocker p-hydroxymercuriphenylsulphonate (pHMPSA). The results show that rheumatoid MNC have significantly impaired ATPase activity compared to healthy cells and that both total and ouabain-sensitive ATPase activities are readily inhibited by pHMPSA. The depressed ATPase activity in rheumatoid MNC could thus be due to blockade/oxidation of a reactive surface thiol, and could contribute to perpetuation of the chronic inflammatory process in these patients.
离子驱动ATP酶在细胞生物学的许多方面发挥着重要作用，包括与慢性炎症相关的单核细胞（MNC）功能。例如，哇巴因是一种Na +、K + ATP酶的特异性抑制剂，它既能抑制T细胞和B细胞的增殖，又能诱导白细胞介素-1的合成。通过微量密度测定法进行细胞化学分析，比较了类风湿关节炎患者和对照受试者的单核细胞中总ATP酶活性和对哇巴因敏感的ATP酶活性。通过与一种非渗透性巯基阻断剂对羟基汞苯磺酸盐（pHMPSA）预孵育，研究了这些酶对巯基阻断试剂失活的敏感性。结果表明，与健康细胞相比，类风湿关节炎患者的单核细胞ATP酶活性显著受损，并且总ATP酶活性和对哇巴因敏感的ATP酶活性都很容易被pHMPSA抑制。因此，类风湿关节炎患者单核细胞中ATP酶活性的降低可能是由于反应性表面巯基的阻断/氧化，并且可能导致这些患者慢性炎症过程的持续存在。
