Institute of Industrial Ecological Sciences, University of Occupational and Environmental Health, Japan.
J Occup Health. 2011;53(4):267-73. doi: 10.1539/joh.l10056. Epub 2011 Jun 13.
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 also associated with oxidative lung injury caused by exposure to potassium octatitanate whiskers (PT1), which is one of the asbestos substitutes.
Male Wistar rats were administered 1 mg or 2 mg PT1 suspended in saline by a single intratracheal instillation and were sacrificed after recovery for 3 days, 1 wk, 1 mo, 3 mo or 6 mo. Gene expression of HO-1 protein and mRNA and immunostaining were investigated in rat lungs.
HO-1 protein expression was increased from 3 days to 1 mo and at 6 mo in the 1 or 2 mg PT1-exposed groups, and the gene expression of HO-1 mRNA was also increased at 3 days and from 1 mo to 6 mo. HO-1-positive cells were mainly found in the alveolar macrophages and the bronchial epithelial cells in immunostaining.
These findings suggest that HO-1 is involved in lung damage caused by PT1.
氧化应激被认为是石棉诱导的肺纤维化的发病机制，血红素加氧酶-1（HO-1）可保护肺组织免受氧化应激。我们假设 HO-1 也与暴露于钛酸钾晶须（PT1）引起的氧化肺损伤有关，PT1 是石棉替代品之一。
雄性 Wistar 大鼠经气管内滴注生理盐水混悬的 1 mg 或 2 mg PT1，分别于染毒后 3 天、1 周、1 个月、3 个月和 6 个月处死。检测大鼠肺组织 HO-1 蛋白和 mRNA 的表达及免疫组化染色。
1 或 2 mg PT1 暴露组大鼠肺组织 HO-1 蛋白表达从 3 天增加到 1 个月，6 个月时仍持续增高，HO-1 mRNA 表达也从 3 天增加到 1 个月到 6 个月时持续增加。免疫组化染色显示 HO-1 阳性细胞主要位于肺泡巨噬细胞和支气管上皮细胞。
这些结果提示 HO-1 参与了 PT1 引起的肺损伤。
