INACTIVATION OF BRONCHIAL MUCOUS PROTEINASE-INHIBITOR BY CIGARETTE-SMOKE AND PHAGOCYTE-DERIVED OXIDANTS
INACTIVATION OF BRONCHIAL MUCOUS PROTEINASE-INHIBITOR BY CIGARETTE-SMOKE AND PHAGOCYTE-DERIVED OXIDANTS
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DOI：
10.3109/01902148009065462
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发表时间：
1980-01-01
影响因子：
1.7
通讯作者：
JANOFF, A
中科院分区：
文献类型：
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作者：
CARP, H;JANOFF, A
新鲜制备的香烟烟雾水溶液抑制支气管粘液（BMPi）和人精浆（HUSI-I）中酸稳定蛋白酶抑制剂的弹性蛋白酶抑制能力（EIC）。经烟雾处理的BMPi和人白细胞弹性蛋白酶的混合物的薄层凝胶免疫过滤分析显示弹性蛋白酶：BMPi复合物减少，未复合的BMPi增加和游离弹性蛋白酶增加。酚类抗氧化剂阻止香烟烟雾对BMPi或HUSI-I的EIC的抑制。用化学氧化剂处理BMPi或HUSI-I引起EIC的类似抑制。用吞噬细胞衍生的氧化系统处理BMPi或HUSI-I，髓过氧化物酶+ H2O + Cl-抑制EIC。与非吸烟者相比，吸烟者气管吸出物中BMPi的功能活性显著降低。结果支持这一假设，即局部失活的BMPi在肺的传导气道吸入香烟烟雾或吞噬细胞衍生的氧化剂可能在吸烟者阻塞性肺疾病的发病机制中发挥作用。
Freshly prepared aqueous solutions of cigarette smoke suppressed elastase inhibitory capacity (EIC) of the acid-stable proteinase inhibitor present in bronchial mucus (BMPi) and human seminal plasma (HUSI-I). Thin-layer gel-immunofiltration analysis of mixtures of smoke-treated BMPi and human leukocyte elastase showed decreased elastase:BMPi complexes, increased uncomplexed BMPi and increased free elastase. Phenolic antioxidants prevented the suppression of the EIC of BMPi or HUSI-I by cigarette smoke. Treatment of BMPi or HUSI-I with chemical oxidants caused a similar suppression of EIC. Treatment of BMPi or HUSI-I with the phagocyte-derived oxidizing system, myeloperoxidase + H2O + Cl- suppressed EIC. Functional activity of BMPi was significantly reduced in tracheal aspirates of human smokers compared to that of nonsmokers. Results support the hypothesis that local inactivation of BMPi in the conducting airways of the lung by inhaled cigarette smoke or by phagocyte-derived oxidants may play a role in the pathogenesis of obstructive lung disease in smokers.