石綿の経気道生体影響とバイオマーカーの検索 : ヘムオキシゲナーゼ-1(HO-1)を中心に [in Japanese] Pulmonary Effect of Asbestosis and Other Particles : Focus on HO-1 Protein Expression [in Japanese]
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It is well known that asbestos induced pulmonary inflammation result in fibrosis. Oxidative stress is thought to be one of the pathogenesis of pulmonary fibrosis, and Heme Oxygenase-1 (HO-1) has been linked to process of protecting lung tissue against oxidative stress. <BR>Heme Oxygenase-1 (HO-1) inducible enzyme that catalyzes heme to generate bilirubin, ferritin, and carbon monoxide (CO) and these resolved products immediately protect lung tissue against oxidative stress. To determine whether or not HO-1 can act as a biomarker of lung injury induced by materials, we made serial measurements of HO-1 expression in rat lungs following the intratracheal instillation of several materials (crocidolite, chrysotile, amosite, crystalline silica) . Male Wistar rats were administered 1 mg or 2 mg of materials suspended in saline by a single intratrachally and were sacrificed at 3 days, 1 week, 1 month, 3 months and 6 months of recovery time. The expression of HO-1 in the rat lung was observed by western blot or ELISA analysis. In case of crocidolite, amosite, chrysotile and crystalline silica which cause sever injury, protein levels of HO-1 in the rat lung constantly increased during the recovery time. The pattern of HO-1 expression is different from materials with severe lung injury and mild or moderate lung injury. It suggests that HO-1 can act as a biomarker of lung injury exposed to particles and fibrous materials.
- Earozoru Kenkyu
Earozoru Kenkyu 23(1), 15-20, 2008-03-20
Japan Association of Aerosol Science and Technology