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Airway epithelial cell changes in rats exposed to 0.25 ppm ozone for 20 months.

作者信息

Ito T, Ikemi Y, Ohmori K, Kitamura H, Kanisawa M

机构信息

Department of Pathology, Yokohama City University School of Medicine, Japan.

出版信息

Exp Toxicol Pathol. 1994 Mar;46(1):1-6. doi: 10.1016/S0940-2993(11)80002-3.

DOI:10.1016/S0940-2993(11)80002-3
PMID:8086780
Abstract

The present study was designed to characterize and quantify morphologic changes occurring in rat intra-pulmonary airway epithelia after long-term exposure to a high ambient level of ozone. Fifteen rats were exposed to 0.25 ppm ozone for 20 months (5 hr/day, 7 days/week) and a control group of 15 rats were exposed to filtered room air. Many intra-cellular brown pigmented granules (presumed to be lipofuscin) were seen in both the control and exposed animals; however, more of these granules were observed in the bronchial and bronchiolar epithelia of the exposed animals. To detect DNA synthesis that occurred in airway epithelial cells during the repair process induced by ozone toxicity, bromodeoxyuridine (BrdU) was injected intraperitoneally one hour before animals were sacrificed; the BrdU-labeling index was evaluated immunohistochemically. There was no difference in the BrdU-labeling index between the groups, the airway epithelia of the ozone-exposed animals exhibiting tolerance to ozone toxicity. However, the epithelial populations in the airways were altered by ozone exposure, and regional differences were seen in the changes. In the exposed animals, mucous cells increased in the lobar bronchus. Calcitonin gene-related peptide-immunoreactive pulmonary endocrine cells and neuroepithelial bodies were more frequently observed in the terminal bronchioles of the exposed animals than in the controls, although there were no differences in the lobar bronchus. Moreover, one adenoma in the peripheral lung was found in the exposed animals, while no tumorous lesions were detected in the controls.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

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