Council for Tobacco Research
Autoradiographic Analysis of Dna Synthesis in Pulmonary Tissues of Mice Exposed to Whole Cigarette Smoke [St Dna Replication Measured in Mice Who Breathed Smoke]
Fields
- Type
- ABSTRACT
- Depository Date
- 31 Jan 1996
- Copied
- Kouri, R.E.,
- Named Person
- Ctr
- Mai
- Kanagalingam, K.K.
- Master ID
- 300200234-0239
- HT0119232-9232 [Enclosed Are Abstracts Discussed Earlier.]
- HT0119233-9233 Studies on the Deposition and Distribution of Catechol From Whole Cigarette Smoke in Bc3f1 Cum Mice [St Effect of Inhaled Catechol on Mice]
- HT0119235-9235 Cigarette Smoke Increases Dna Replication in Lung and Sister Chromatid Exchange (Sce) in Bone Marrow of Mice [St Mice Studied After Nose Only Inhalation]
- HT0119236-9236 the Effect of Exposure to Whole Cigarette Smoke on Short-Term Endpoints in Bc3f1 Cum Mice. [St Test Involving Mice Who Inhaled Nose Only Smoke]
- HT0119237-9237 the Effect of Lifetime Exposure to Whole Cigarette Smoke in Bc3f1 Cum Mice [St Study Involving Nose Only Exposure with Mice]
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A1ITORADIOGRAI'I1IC ANALYSIS OF DNA SYNTHESIS IN PUL-
MONARY TISSUES OF MICE EXPOSED TO WHOLE CIGARETTE
SMOKE. K.K. Kanagalingam, S.M. Reed, D.R. Dansie,
W.C. 71-i11, R.E. Kouri, and C.J. Henry, Dept. of
Experimental Oncology, Micro4iological Associates,
5221 River Road, Bethesda, MD 20816-1493
DNA replication, as measured by estimation of
Labeling Index (LI), was determined in BC3FI/Cum
mice after daily exposure to whole cigarette mnoke
over a 12 month period. Imxeediately following the
last smuke-exposure, lung DNA was labeled with a
1.0 hr. pulse of tritieted thymidine (3H-TdR) and
tissues processed for autoradiography. LI in
smoke-exposed mice was increased over controls
after 9 weeks of exposure. This increase per-
sisted over the entire study period. Of the 4000-
6000 cells counted in both sham-exposed and shelf-
control mice, not more than 3 cells had any signi-
ficant number of grains. The percent of total
cells labeled after 13 weeks was about 20-fold and
14-fold greater in mice exposed to smoke from 3A1
and 2R1 cigarettes, respectively. In the smoke-
exposed lung, the distribution of cells with
grains was regular. No labeling of cells of the
bronchial epithelium was found, rather the uptake
of 3H-TdR was confined to alveolar cells. Neither
necrosis nor epithelial hyperplasia was observed
in any area of the lung that would account for the
increase in LI. A high percentage (ti679:) of cells
in the smoke-exposed mice wera labeled with less
than 30 grains per nucleus. In contrast, in the
control mice only about 35% of the total cells
contained less than 30 grains per nucleus. This
low grain number is•generally indicative of DNA
repair synthesis. Thus, these data suggest that
whole cigarette smoke, while stimulating normal
DNA replication may induce unscheduled or DNA re-
pair synthesis as well.
Supported by The Council for Tobacco Research-USA,
Inc.
Inhalation; Industrial; Pulmonary
HTQ0119234
Dr. Ken K. Kanagalingam
Dept. of Experimental Oncology
Microbiological Associates
5221 River Road
Bethesda, MD 20816-1493
(301) 654-3400
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