Oxidative stress is thought to be the pathogenesis of pulmonary fibrosis induced by particles, and heme oxygenase-1 (HO-1) protects lung tissue against oxidative stress. We hypothesized that HO-1 is also associated with oxidative lung injury caused by exposure to particles. The present study was conducted to investigate the time course of HO-1 expression of lungs exposed to crystalline silica in vivo. Male Wistar rats were administered 1 mg or 2 mg of crystalline silica suspended in saline by a single intratracheal instillation and were sacrificed at 3 d, 1 wk, 1 month, 3 months and 6 months of recovery time. The expression of HO-1 was observed by western blot analysis and immunostaining. Protein levels of HO-1 were increased compared to the controls at 3 d, and from 1 month to 6 months following intratracheal instillation of 2 mg of crystalline silica. The levels of HO-1 were increased compared to the controls from 1 month to 6 months following intratracheal instillation of 1 mg of crystalline silica. Many HO-1 positive cells were found particularly in the alveolar macrophages during immunostaining. These findings suggest that HO-1 is related to lung injury arising from exposure to crystalline silica.
CITATION STYLE
Nagatomo, H., Morimoto, Y., Oyabu, T., Hirohashi, M., Ogami, A., Yamato, H., … Tanaka, I. (2006). Expression of heme oxygenase-1 in the lungs of rats exposed to crystalline silica. Journal of Occupational Health, 48(2), 124–128. https://doi.org/10.1539/joh.48.124
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