McLemore T L, Martin R R, Toppell K L, Busbee D L, Cantrell E T
J Clin Invest. 1977 Nov;60(5):1017-24. doi: 10.1172/JCI108852.
Aryl hydrocarbon hydroxylase induction was studied in cultured peripheral blood lymphocytes and pulmonary alveolar macrophages from 15 smokers and 8 nonsmokers with a variety of pulmonary diseases. Enzyme levels in lymphocytes from cigarette smokers cultured in medium without an inducing agent were 57+/-6 mU/10(6) cells (mean+/-SEM), while enzyme levels in lymphocytes from nonsmokers were 20+/-2 mU/10(6) cells (P < 0.001). When lymphocytes were cultured in the presence of the inducing agent, benzo-(a)anthracene, enzyme activity was increased to 168+/-23 mU/10(6) cells in smokers' cells and 99+/-22 mU/10(6) cells in lymphocytes from nonsmokers (P < 0.04). When noninduced enzyme values in cultured macrophages were compared, smokers' cells had enzyme levels of 45+/-5 mU/10(6) cells, whereas nonsmokers had enzyme activity of 24+/-2 mU/10(6) cells (P < 0.002). However, pulmonary macrophages from smokers or nonsmokers, cultured in the presence of benzo(a)-anthracene, had similar levels of induced enzyme activity (P > 0.1). A positive correlation was observed for nonsmokers (r = 0.596, P > 0.1 <0.2) or smokers (r = 0.640, P < 0.04), when enzyme values for noninduced cultures of macrophages and lymphocytes from individual patients were simultaneously compared. Enzyme values for macrophages and lymphocytes cultured in the presence of an inducer also revealed a positive correlation for individual smokers (r = 0.801, P < 0.001) or nonsmokers (r = 0.785, P < 0.01). Inducibility (expressed as fold-induction) for macrophages and lymphocytes from individual patients was also positively correlated (r = 0.889, P < 0.001 for nonsmokers and r = 0.942, P < 0.001 for smokers). These results indicate that the capacity for aryl hydrocarbon hydroxylase induction is similar whether tested in lymphocytes or pulmonary macrophages from this group of pulmonary disease patients.
对15名吸烟者和8名患有各种肺部疾病的非吸烟者的外周血淋巴细胞和肺泡巨噬细胞进行培养,研究芳烃羟化酶的诱导情况。在无诱导剂的培养基中培养的吸烟者淋巴细胞中的酶水平为57±6 mU/10⁶细胞(平均值±标准误),而非吸烟者淋巴细胞中的酶水平为20±2 mU/10⁶细胞(P<0.001)。当淋巴细胞在诱导剂苯并(a)蒽存在下培养时,吸烟者细胞中的酶活性增加到168±23 mU/10⁶细胞,非吸烟者淋巴细胞中的酶活性增加到99±22 mU/10⁶细胞(P<0.04)。比较培养的巨噬细胞中未诱导的酶值时,吸烟者细胞的酶水平为45±5 mU/10⁶细胞,而非吸烟者的酶活性为24±2 mU/10⁶细胞(P<0.002)。然而,吸烟者或非吸烟者的肺巨噬细胞在苯并(a)蒽存在下培养时,诱导的酶活性水平相似(P>0.1)。当同时比较个体患者巨噬细胞和淋巴细胞未诱导培养物的酶值时,非吸烟者(r = 0.596,P>0.1<0.2)或吸烟者(r = 0.640,P<0.04)均观察到正相关。在诱导剂存在下培养的巨噬细胞和淋巴细胞的酶值在个体吸烟者(r = 0.801,P<0.001)或非吸烟者(r = 0.785,P<0.01)中也显示出正相关。个体患者巨噬细胞和淋巴细胞的诱导性(以诱导倍数表示)也呈正相关(非吸烟者r = 0.889,P<0.001;吸烟者r = 0.942,P<0.001)。这些结果表明,在这组肺部疾病患者的淋巴细胞或肺巨噬细胞中测试时,芳烃羟化酶的诱导能力相似。