Induction of Aryl Hydrocarbon Hydroxylase in Human Pulmonary Alveolar Macrophages by Cigarette Smoking

E. T. Cantrell; G. A. Warr; D. L. Busbee; R. R. Martin

doi:10.1172/JCI107371

^{Department of Biology, M. D. Anderson Hospital and Tumor Institute, Houston, Texas 77025}

^{Department of Medicine, Baylor College of Medicine, Houston, Texas 77025}

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^{Department of Biology, M. D. Anderson Hospital and Tumor Institute, Houston, Texas 77025}

^{Department of Medicine, Baylor College of Medicine, Houston, Texas 77025}

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^{Department of Biology, M. D. Anderson Hospital and Tumor Institute, Houston, Texas 77025}

^{Department of Medicine, Baylor College of Medicine, Houston, Texas 77025}

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^{Department of Biology, M. D. Anderson Hospital and Tumor Institute, Houston, Texas 77025}

^{Department of Medicine, Baylor College of Medicine, Houston, Texas 77025}

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Published in Volume 52, Issue 8 on August 1, 1973
J Clin Invest. 1973;52(8):1881–1884. https://doi.org/10.1172/JCI107371.
© 1973 The American Society for Clinical Investigation

Published August 1, 1973 - Version history

Pulmonary alveolar macrophages were obtained from healthy volunteers by saline pulmonary lavage, and aryl hydrocarbon hydroxylase was measured in the cells. Enzyme activity was low in cells from five nonsmokers with a mean of 0.008±0.004 U/10⁶ cells. Cells obtained from nine cigarette smokers contained higher enzyme levels, with a mean of 0.095±0.024 U/10⁶ cells. A former cigarette smoker was lavaged on five occasions. Enzyme activity during two lavages 4 mo apart were 0.010 and 0.009 U/10⁶ cells, respectively. 1 wk after smoking was resumed, the enzyme activity rose slightly to 0.013, and reached 0.041 U/10⁶ cells by 1 mo. Upon cessation of smoking, the enzyme activity returned to control levels by the next lavage, 2 mo later. These data indicate that aryl hydrocarbon hydroxylase may be induced in pulmonary alveolar macrophages of subjects chronically exposed to cigarette smoke.

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