Abstract
A single injection of urethane into adult male A2G mice produced an increase in the proliferative rate of alveolar wall cells, reaching a peak at 2 weeks post urethan (PU) and declining to control levels by 2 months PU. During this urethane induced proliferative response the single and double labelling indices and the native metaphase index were all elevated although there was no corresponding alteration in the arrested metaphase index. This proliferative response may not be restricted to hyperplasia of potentially neoplastic cells, such as type II epithelium, but may also include type I epithelial cells and alveolar macrophage precursors. However, it was impossible to identify individual cell populations by methods used. The growth rate of adenomata decrease with time and cell kinetic techniques showed that the rates of entry of adenoma cells into DNA synthesis and into metaphase were decreasing concurrently with the growth rate. Thus the rate of cell production falls as adenomata age but how much cell loss contributes to the decrease in growth rate is not yet known. Decreasing cell production could be due to an increased cell cycle time and/or a decreased growth fraction. The duration of DNA synthesis in adenomata increased markedly as the mice survived, suggesting that the cell cycle time might be increased, but further experiments are required to determine whether the growth fraction changes. Attention is drawn to a complication that Colcemid introduces into kinetic studies on alveolar wall cells.
Highlights
Summary.-A single injection of urethane into adult male A2G mice produced an increase in the proliferative rate of alveolar wall cells, reaching a peak at 2 weeks post urethane (PU) and declining to control levels by 2 months PU
Attention is drawn to a complication that Colcemid introduces into kinetic studies on alveolar wall cells
THE DISCOVERY by Nettleship, Henshaw and Meyer (1943) that urethane treatment increased the incidence of pulmonary adenomata in A strain mice prompted its use as a model of tumorigenesis by many investigators, but most studies merely relied on enumeration of surface adenomata
Summary
Male specific pathogen-free (SPF) A2G mice were obtained in batches from the Laboratory Animals Centre, Carshalton, over a period of about 12 months. The between kB and the observed growth other experimental and control subgroups rate (kG) obtained by direct measurement of the tumours Such computations assume a steady flow of cells through the cell cycle with no diurnal effects, that Colcemid (demecolcine) does not affect labelling, that all tumour growth is due to mitotic division and that all cells did not receive Colcemid but were given 2 3H-Tdr injections, one at 13.00 h and the other at 14.00 h before killing at 14.30 h. To increase the precision of the growth curve of surface adenomata, it was necessary to interpolate comparable groups of 10 SPF derived male A2G mice at intervals of 7-5, 22-5 and 32-5 weeks post urethane entering DNA synthesis subsequently (PU) All these mice received a single enter mitosis. Index of the size of the adenomata was obtained by measuring 2 horizontal diameters
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
