DNA synthesis in pulmonary alveolar macrophages and type II cells: Effects of ozone exposure and treatment with α‐difluoromethylornithine
- 30 April 1987
- journal article
- research article
- Published by Taylor & Francis in Journal of Toxicology and Environmental Health
- Vol. 21 (1-2) , 15-26
- https://doi.org/10.1080/15287398709530999
Abstract
An increase in the number of pulmonary alveolar macrophages (AM) can be induced by a number of toxic insults to the lung, including ozone, an important photochemical oxidant air pollutant. This increase could arise from an influx of monocytes from the vascular or interstitial compartments, or from proliferation of AM in situ. While proliferation of alveolar type II cells after oxidant exposure has been well documented, it is not clear whether AM are also capable of this response. Rats were exposed to air or to 0.12, 0.25, or 0.50 ppm ozone for 1, 2, 3, 7, or 14 d, 20 hid. The labeling index in both AM and type II cells increased about 10‐fold after 2 d of exposure to 0.25 and 0.50 ppm of ozone, but returned to control levels by the end of 1 wk of exposure. These changes closely paralleled the temporal and dose‐response characteristics of changes in total lung DNA synthesis. α‐Difluoromethylornithine (DFMO) administered to rats during a 2‐d exposure to 0.50 ppm ozone did not inhibit the ozone‐induced increase in labeling index in AM or type II cells, although evidence of inhibition of lung ornithine decarboxylase activity was obtained, and the ozone‐induced increase in total lung DNA synthesis was inhibited by 23%. These results suggest that, like type II cells, AM are capable of entering the cell cycle and synthesizing new DNA in situ in response to short‐term exposure to environmentally relevant doses of ozone, and that the ozone‐induced stimulation of DNA synthesis in these cell types was refractory to inhibition by DFMO.This publication has 38 references indexed in Scilit:
- Effects of Short-Term Exposure to Diesel Exhaust on Lung Cell Proliferation and Phospholipid MetabolismExperimental Lung Research, 1986
- Alveolar macrophage replication. One mechanism for the expansion of the mononuclear phagocyte population in the chronically inflamed lung.Journal of Clinical Investigation, 1984
- Alterations in lung structure caused by inhalation of oxidantsJournal of Toxicology and Environmental Health, 1984
- Polyamine metabolism in rat lungs with oxygen toxicityBiochemical and Biophysical Research Communications, 1983
- Morphometry of In Situ and Lavaged Pulmonary Alveolar Macrophages from Control and Ozone-Exposed RatsExperimental Lung Research, 1983
- Changes in pulmonary phospholipid biosynthetic enzymes after nitrogen dioxide exposureToxicology and Applied Pharmacology, 1981
- Origin, Kinetics, and characteristics of pulmonary macrophages in the normal steady state.The Journal of Experimental Medicine, 1979
- Effect of α-difluoromethylornithine, an enzyme-activated irreversible inhibitor of ornithine decarboxylase, on polyamine levels in rat tissuesLife Sciences, 1979
- Ultraviolet Light Induces Epidermal ornithine Decarboxylase ActivityJournal of Investigative Dermatology, 1978
- Direct Evidence for a Bone Marrow Origin of the Alveolar Macrophage in ManScience, 1976