| Literature DB >> 15814490 |
Hiroko Nagatomo1, Yasuo Morimoto, Takako Oyabu, Masami Hirohashi, Akira Ogami, Hiroshi Yamato, Kaori Kuroda, Toshiaki Higashi, Isamu Tanaka.
Abstract
Oxidative stress is thought to be the pathogenesis of pulmonary fibrosis induced by asbestos, and heme oxygenase-1 (HO-1) protects lung tissue against oxidative stress. We hypothesized that HO-1 is associated with oxidative lung injury caused by exposure to asbestos. This study was conducted to investigate the time course of HO-1 expression of lungs exposed to crocidolite asbestos in vivo. Male Wistar rats were administered 1 mg or 2 mg crocidolite asbestos suspended in saline by a single intratracheal instillation and were sacrificed at 3 d, 1 wk, 1 mo, 3 mo, and 6 mo of recovery time. The expression of HO-1 was observed by Western blot analysis and immunostaining. Protein levels of HO-1 increased at from 3 d to 6 mo following intratracheal instillation of 2 mg crocidolite asbestos. The levels of HO-1 increased at 1 wk and 1 mo following intratracheal instillation of 1 mg crocidolite asbestos. Many HO-1-positive cells were found, particularly in the alveolar macrophages, during immunostaining. These findings suggest that HO-1 may be related to lung disorder induced by dust and therefore can act as a biomarker of lung injury due to dust exposure.Entities:
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Year: 2005 PMID: 15814490 DOI: 10.1080/08958370590922580
Source DB: PubMed Journal: Inhal Toxicol ISSN: 0895-8378 Impact factor: 2.724