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American Journal of Pathology, Vol 136, 1293-1299, Copyright © 1990 by American Society for Investigative Pathology
REGULAR ARTICLES |
DW Wilson and HJ Segall
Department of Pathology and Pharmacology, University of California- Davis 95616.
Unlike many other systemically administered pneumotoxicants affecting alveolar septa, Monocrotaline (MCT) does not cause a proliferative type II cell response. To determine whether MCT has an effect that might alter the type II cell response, we determined the numerical density and volume of type II cells in lungs from MCT-treated rats. Morphometric parameters were derived from estimates of nuclear volume based on point and intercept ratios counted in electron micrographs of type II cell profiles. These were combined with point and intercept counts of alveolar septal structures and counts of nuclear profiles per unit area to calculate average cell volume and numerical density of type II cells. Areal densities of type II cell profiles were determined by light microscopic counts of alveolar parenchyma and normalized to the volume of lung parenchyma. Cell volume of type II cells was markedly increased in MCT-treated animals (1.25 X 10(3) microns3) compared with controls (3.4 X 102) microns3). Nuclear diameter of type II cells was similarly increased (8.53 microns in treated animals versus 5.81 microns in controls). The number of type II cells was markedly decreased in treated animals (1.36 X 10(6] cells per cm3 lung parenchyma compared with 7.65 X 10(6) cells per cm3 parenchyma in controls). We conclude that MCT causes marked cellular hypertrophy of type II alveolar epithelial cells and that this hypertrophy is somehow related to a failure to maintain normal cell populations in the lung of MCT-treated rats. We hypothesize that this change is analogous to the hypertrophy and mitotic inhibition that occurs in the liver of animals treated with hepatotoxic pyrrolizidine alkaloids.
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