Aryl hydrocarbon hydroxylase in lymphocytes and lung tissue from lung cancer patients and controls

Abstract

The inducibility of aryl hydrocarbon hydroxylase (AHH) activity in peripheral mitogen‐treated lymphocytes, and of AHH and other monoxygenase activities in lung samples, was studied in 41 patients–34 with pulmonary carcinoma, 4 with a benign lung tumour and 3 with chronic obstructive pulmonary disease. Lymphocyte AHH induction alone was studied in 43 non‐smoking and 37 smoking surgical patients. Absolute induced and non‐induced AHH activities were at about the same level in the lymphocytes from the lung cancer patients as in those from the non‐smoking controls, whereas the activities in smoking controls were about 100% higher. The mean inducibility ratios were very similar in all groups, ranging from 4.4 in the benign tumour patients to 5.4 in both control groups. Thymidine incorporation was on average about 40% lower in the lymphocytes from the lung cancer patients. AHH activity was detectable in all the peripheral lung samples, both normal or tumorous tissue, and its inter‐individual variation was more than 67‐fold. ECDE activity was also detectable in all the samples studied and its correlation with AHH activity was statistically significant (r = 0.888), suggesting that the same enzyme metabolizes both substrates. ERDE was detectable only in the samples with the highest AHH and ECDE activities. There was no correlation between basal or induced lymphocyte AHH activities and lung tissue AHH activity, but there were statistically significant correlations between lung AHH activity and the inducibility ratio with (r = 0.618) or without correction by thymidine incorporation (r = 0.442). These correlations suggest that there are common regulatory factors for AHH inducibility in different tissues. No significant difference in any drug metabolism parameter measured was observed between the lung cancer patients and the controls.