Cytogenetic effects of cigarette smoke on pulmonary alveolar macrophages of the rat

• Published in: Environmental and molecular mutagenesis Vol. 14; no. 1; p. 27
• Main Authors: Rithidech, K, Chen, B T, Mauderly, J L, Whorton, Jr, E B, Brooks, A L
• Format: Journal Article
• Language: English
• Published: United States 1989
• Subjects: Animals; Bone Marrow - ultrastructure; Chromosome Aberrations; Macrophages - drug effects; Macrophages - ultrastructure; Male; Nicotiana; Plants, Toxic; Pulmonary Alveoli - drug effects; Pulmonary Alveoli - ultrastructure; Rats; Rats, Inbred F344; Smoke - adverse effects
• ISSN: 0893-6692
• DOI: 10.1002/em.2850140106

To determine accurately the potential genetic damage induced by toxic inhaled agents, the cells that receive a high concentration of such agents should be analyzed. Pulmonary alveolar macrophages (PAMs) represent such cells. We compared the cytogenetic effects of cigarette smoke on PAMs of rats exposed repeatedly by different methods. This study was part of a larger investigation of the health effects resulting from different methods of exposing rats to cigarette smoke. Fischer 344/N male rats (4/group) were randomly selected from five different exposure groups: 1) nose-only sham-exposed (air) control, 2) whole-body sham-exposed control, 3) nose-only intermittent, 4) nose-only continuous, and 5) whole-body continuous. The rats were exposed 6 hr/day, 5 days/week for 22-24 days. All smoke-exposed rats received the same daily concentration x time product (600 mg.hr.m-3 for the first week, 1200 mg.hr.m-3 thereafter) of cigarette smoke. Rats were injected intraperitoneally with colchicine at the end of exposure. PAMs were obtained by lung lavage and chromosomal damage was measured. Highly significant smoke-induced differences in both structural and numerical aberrations were observed in continuously exposed rats vs. sham controls, regardless route of exposure. The structural aberrations observed were chromatid-type deletions. Both hypoploid and hyperploid cells were detected. Our data suggest that cigarette smoke is clastogenic and may disrupt spindle-fiber formation. These activities may play a role in the induction of human carcinogenesis caused by cigarette smoke exposure.