Analysis of aryl hydrocarbon hydroxylase activity in human lung tissue, pulmonary macrophages, and blood lymphocytes.

Abstract

Aryl hydrocarbon hydroxylase (AHH) activity was measured fluorometrically in surgically-excised fresh lung tissue, pulmonary alveolar macrophages (PAMs), and peripheral blood lymphocytes from 14 cigarette smokers (7 with and 7 without primary lung cancer). Levels of AHH in fresh PAMs and AHH inducibility (expressed as fold-induction) in cultured, mitogen-stimulated lymphocytes from individual noncancer patients correlated well (r =0.975, p < 0.001). For individual lung cancer patients, however, these values were dissociated (linear regression not appropriate for this set of values). Levels of AHH in fresh lung tissue and fold-induction ratios in cultured lymphocytes from individual noncancer patients also exhibited a positive correlation (r =0.976, p < 0.001), while values for individual lung cancer patients did not (r =0.007, p =0.987). A close agreement was noted for AHH in fresh lung tissue and fresh PAMs from individual noncancer patients (r =0.984, p < 0.001), while these values are weakly correlated for lung cancer patients (r =0.658, p < 0.11). When AHH activity in fresh PAMs, in fresh lung tissue, and AHH inducibility in cultured lymphocytes were simultaneously compared, an excellent relationship was observed for values for all 3 tissues for individual noncancer patients (r =0.987, p < 0.001). However, AHH levels in these 3 tissues from individual lung cancer patients were not correlated (r =0.701, p > 0.25). These results indicate similar capacity for AHH induction is present in fresh lung tissue, fresh PAMs, and cultured mitogen-stimulated lymphocytes from cigarette smokers without evidence of lung cancer, but AHH values are not positively correlated with similar tissues from individual lung cancer patients.