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Title DNA synthesis in pulmonary alveolar macrophages and type II cells: effects of ozone exposure and treatment with -difluoromethylornithine
Creator/Author Wright, E.S. ; White, D.M. ; Brady, A.N. ; Li, L.C. ; D`Arcy, J.B. ; Smiler, K.L.
Publication Date1987 Jan 01
OSTI IdentifierOSTI ID: 6409687
Other Number(s)CODEN: JTEHD
Resource TypeJournal Article
Resource RelationJ. Toxicol. Environ. Health ; Vol/Issue: 21:1-2
Research OrgGeneral Motors Research Labs., Warren, MI
Subject560300 -- Chemicals Metabolism & Toxicology; MACROPHAGES-- DNA REPLICATION;ORGANIC FLUORINE COMPOUNDS-- BIOLOGICAL EFFECTS;OZONE-- TOXICITY; ANIMAL CELLS;CELL CYCLE;DOSE-RESPONSE RELATIONSHIPS;LUNGS;RATS;STIMULATION
Related SubjectANIMAL CELLS;ANIMALS;BODY;CONNECTIVE TISSUE CELLS;MAMMALS;NUCLEIC ACID REPLICATION;ORGANIC COMPOUNDS;ORGANIC HALOGEN COMPOUNDS;ORGANS;PHAGOCYTES;RESPIRATORY SYSTEM;RODENTS;SOMATIC CELLS;VERTEBRATES
Description/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 h/d.^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.^ -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.
Country of PublicationUnited States
LanguageEnglish
FormatPages: 15-26
System Entry Date2001 May 13

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