| Chrysotile asbestos causes AEC apoptosis via the caspase activation in vitro and in vivo. | |
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MedLine Citation:
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PMID: 18300051 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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To determine whether alveolar epithelial cell (AEC) apoptosis via caspase activation is involved in asbestos-induced lung injury, we examined apoptosis, caspase-3 and-9 activation using chrysotile asbestos exposure models in vitro and in vivo. Apoptotic cells were assessed in A549 cells with terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) method after 48 hours exposure of chrysotile asbestos (5 to 100 ug/cm2). Asbestos exposure induced a dose-dependent increase of apoptotic cells, and both pretreatment with Z-LEHD-FMK (caspase-3 inhibitor) or Z-DEMK-FMK (caspase-9 inhibitor) significantly suppressed asbestos-induced apoptosis. Expression of cleaved caspase-3 and-9 increased significantly from 18 to at least 48 hours after asbestos exposure. In vivo study, either 1 or 2 mg of chrysotile asbestos were administered into rat lungs intratracheally, and the lungs were obtained 3 days, 1 and 2 weeks, 1, 3 and 6 months after the administration. Asbestos exposure increased the number of apoptotic cells and the activation of cleaved caspase-3 and -9 most at 3 days in a dose dependent manner, and continued to increase them until at least 6 months after asbestos exposure. Apoptotic cells and cleaved caspase-3 and -9 positive cells were mainly observed in AECs. These findings suggest that AEC apoptosis via caspase-3 and -9 activation is involved in asbestos-induced lung injury. |
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Authors:
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Takashi Kido; Yasuo Morimoto; Etsuko Asonuma; Kazuhiro Yatera; Akira Ogami; Takako Oyabu; Isamu Tanaka; Masamitsu Kido |
Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Inhalation toxicology Volume: 20 ISSN: 1091-7691 ISO Abbreviation: Inhal Toxicol Publication Date: 2008 Feb |
Date Detail:
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Created Date: 2008-02-26 Completed Date: 2008-03-13 Revised Date: 2009-11-03 |
Medline Journal Info:
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Nlm Unique ID: 8910739 Medline TA: Inhal Toxicol Country: United States |
Other Details:
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Languages: eng Pagination: 339-47 Citation Subset: IM |
Affiliation:
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Department of Respiratory Disease, University of Occupational and Environmental Health, Fukuoka, Japan. t-kido@med.uoeh-u.ac.jp |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Air Pollutants
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toxicity* Animals Apoptosis / drug effects* Asbestos, Serpentine / toxicity* Blotting, Western Caspase 3 / antagonists & inhibitors, metabolism* Caspase 9 / antagonists & inhibitors, metabolism* Cell Count Cell Line, Transformed Cells, Cultured Dose-Response Relationship, Drug Enzyme Activation / drug effects Enzyme Inhibitors / pharmacology Fluorescent Antibody Technique, Direct Granuloma, Foreign-Body / chemically induced, pathology Humans Immunoenzyme Techniques In Situ Nick-End Labeling Intubation, Intratracheal Lung / drug effects, enzymology, pathology Male Particle Size Pulmonary Alveoli / drug effects*, enzymology, pathology Rats Rats, Wistar |
| Chemical | |
Reg. No./Substance:
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0/Air Pollutants; 0/Asbestos, Serpentine; 0/Enzyme Inhibitors; EC 3.4.22.-/Caspase 3; EC 3.4.22.-/Caspase 9 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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