Zur Bedeutung von Apoptose und Proliferation bei Stickstoffdioxid-Exposition der Lunge
Die chronisch obstruktive Lungenerkrankung und das Lungenemphysem werden weltweit mit steigender Tendenz diagnostiziert. Als Hauptursache für die Entwicklung eines Emphysems wird das Zigarettenrauchen verantwortlich gemacht. Doch bisher ist nicht klar, wie der Zigarettenrauch die Lunge schädigt und...
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| Format: | Doctoral Thesis |
| Language: | German |
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Philipps-Universität Marburg
2007
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| Online Access: | PDF Full Text |
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We hypothesize that increased apoptosis of alveolar wall cells results in emphysema in an inhalation model. Male Fischer 344 rats (n=4-7/group) were exposed to room air containing 10ppm NO2 for 3, 7, 21, or 21 days followed by 28d at room air. Age-matched rats were exposed to room air. Lungs were fixed by instillation at 20cm H2O. Uniform systematic random samples were embedded into paraffin and methacrylate. Levels of apoptosis (TUNEL) and proliferation (Ki67), airspace enlargement and alveolar surface area were determined by stereology. Apoptosis was increased at days 3, 7 in NO2. Proliferation was increased at day 3 only. Volume-weighted mean alveolar volume was higher at days 7, 21 in NO2, and after recovery in comparison with controls d3, d7, but not with controls d49. Alveolar surface area steadily increased to values achieved in controls by day 49. We suggest that apoptosis is related to increased cell turnover due to NO2-exposure, which appears to accelerate parenchymal growth or aging.