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Changes in type II cell populations in monocrotaline pneumotoxicity
1Department of Pathology and Pharmacology, University of California-Davis 95616.
The American Journal of Pathology
|June 1, 1990
Summary
Monocrotaline (MCT) causes significant cellular hypertrophy in type II alveolar epithelial cells, leading to decreased cell numbers in rat lungs. This suggests MCT alters normal lung cell populations.
Area of Science:
- Pulmonary toxicology
- Cell biology
- Respiratory pathology
Background:
- Systemic pneumotoxicants typically induce a proliferative type II cell response.
- Monocrotaline (MCT) is a pneumotoxicant known not to elicit this proliferative response.
Purpose of the Study:
- To investigate the effect of Monocrotaline (MCT) on type II alveolar epithelial cells.
- To determine if MCT alters the numerical density and volume of type II cells in rat lungs.
Main Methods:
- Utilized morphometric analysis of electron micrographs from MCT-treated and control rat lungs.
- Calculated average cell volume and numerical density of type II cells using point and intercept counts.
- Determined areal densities of type II cell profiles via light microscopy.
Main Results:
- MCT treatment caused a marked increase in type II cell volume (1.25 x 10^3 µm³ vs. 3.4 x 10² µm³).
- Nuclear diameter of type II cells was significantly larger in MCT-treated rats (8.53 µm vs. 5.81 µm).
- Numerical density of type II cells decreased significantly in MCT-treated rats (1.36 x 10⁶ cells/cm³ vs. 7.65 x 10⁶ cells/cm³).
Conclusions:
- Monocrotaline (MCT) induces significant cellular hypertrophy of type II alveolar epithelial cells.
- This hypertrophy is linked to a failure in maintaining normal type II cell populations in MCT-treated rat lungs.
- Hypothesized that MCT-induced changes are analogous to liver hypertrophy and mitotic inhibition seen with hepatotoxic pyrrolizidine alkaloids.