TY - JOUR
T1 - Dissociation between Aryl Hydrocarbon Hydroxylase Activity in Cultured Pulmonary Macrophages and Blood Lymphocytes from Lung Cancer Patients
AU - McLemore, Theodore L.
AU - Wray, Nelda
AU - Cantrell, Elroy T.
AU - Busbee, David L.
PY - 1978/11/1
Y1 - 1978/11/1
N2 - The in vitro induction of aryl hydrocarbon hydroxylase was measured in pulmonary alveolar macrophages and peripheral blood lymphocytes from 14 cigarette smokers with primary lung cancer and 15 smokers with a variety of nonneoplastic pulmonary diseases. Enzyme levels were measured in cells cultured with or without the inducer benzathracene. For both induced and noninduced cultures, there were no differences in mean levels of cultured macrophage or lymphocyte enzyme activity between noncancer and lung cancer patients. Absolute levels and fold induction of aryl hydrocarbon hydroxylase in cultured macrophages and lymphocytes from individual noncancer patients were positively correlated [noninduced (r=0.640, p<0.04), induced (r=0.801, p<0.001), and fold induction (r=0.942, p<0.001)]. However, comparison of these values in cultured macrophages and lymphocytes from individual lung cancer patients demonstrated no positive correlation [noninduced (r=0.083, p>0.3), induced (r=0.306, p>0.3), and fold induction (r=-0.625, p<0.02)]. Comparison of enzyme activity in macrophages freshly lavaged from the lung and benzanthracene-induced activity in cultures macrophages revealed a positive correlation for both noncancer (r=0.865, p<0.005) and lung cancer (r=0.971; p<0.001) patients. Similarly, comparison of enzyme activity in fresh macrophages and fold induction values in cultured macrophages was also well correlated for both groups of patients (r=0.876, p<0.001 for non-cancer patients; r=0.908, p<0.001 for lung cancer patients). Multivariant analysis of enzyme characteristics in several tissues may be useful in lung cancer diagnosis and in assessment of lung cancer risk. However, the use of a single tissue such as lymphocytes for evaluation of the relationship between aryl hydrocarbon hydroxylase activity and cancer susceptibility is questionable.
AB - The in vitro induction of aryl hydrocarbon hydroxylase was measured in pulmonary alveolar macrophages and peripheral blood lymphocytes from 14 cigarette smokers with primary lung cancer and 15 smokers with a variety of nonneoplastic pulmonary diseases. Enzyme levels were measured in cells cultured with or without the inducer benzathracene. For both induced and noninduced cultures, there were no differences in mean levels of cultured macrophage or lymphocyte enzyme activity between noncancer and lung cancer patients. Absolute levels and fold induction of aryl hydrocarbon hydroxylase in cultured macrophages and lymphocytes from individual noncancer patients were positively correlated [noninduced (r=0.640, p<0.04), induced (r=0.801, p<0.001), and fold induction (r=0.942, p<0.001)]. However, comparison of these values in cultured macrophages and lymphocytes from individual lung cancer patients demonstrated no positive correlation [noninduced (r=0.083, p>0.3), induced (r=0.306, p>0.3), and fold induction (r=-0.625, p<0.02)]. Comparison of enzyme activity in macrophages freshly lavaged from the lung and benzanthracene-induced activity in cultures macrophages revealed a positive correlation for both noncancer (r=0.865, p<0.005) and lung cancer (r=0.971; p<0.001) patients. Similarly, comparison of enzyme activity in fresh macrophages and fold induction values in cultured macrophages was also well correlated for both groups of patients (r=0.876, p<0.001 for non-cancer patients; r=0.908, p<0.001 for lung cancer patients). Multivariant analysis of enzyme characteristics in several tissues may be useful in lung cancer diagnosis and in assessment of lung cancer risk. However, the use of a single tissue such as lymphocytes for evaluation of the relationship between aryl hydrocarbon hydroxylase activity and cancer susceptibility is questionable.
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M3 - Article
C2 - 698938
AN - SCOPUS:0018180241
SN - 0008-5472
VL - 38
SP - 3805
EP - 3811
JO - Cancer research
JF - Cancer research
ER -