首页> 美国卫生研究院文献>British Journal of Experimental Pathology >Lung injury: cell-specific bioactivation/deactivation of circulating pneumotoxins.
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Lung injury: cell-specific bioactivation/deactivation of circulating pneumotoxins.

机译:肺损伤:循环性肺毒素的细胞特异性生物激活/失活。

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摘要

Many of the blood-borne xenobiotics which result in injury to the lung are not inherently pneumotoxic but cause damage within the target cells following metabolic activation. This injury is usually restricted to those cells capable of bioactivation and thus, in addition to its clinical significance, it provides a valuable indicator of the normal metabolic activity within the numerous cell types present in lung. Not surprisingly, injury does not simply reflect the presence or absence of a particular enzyme but rather the balance between mechanisms for activation and deactivation. A change in the balance between different enzymes may also determine whether activation results in injury or tumorigenesis (Foster et al. 1992). Changes in particular types of cells cannot be determined by analysing whole lung homogenates. Isolation of particular cell types can provide valuable information but this approach does not address the differences between adjacent cells of the same type (Forkert & Moussa 1989; Dinsdale et al. 1992). Further progress may require the correlation of the injury with the status of individual cells; the quantitation of histochemical and immunocytochemical data is notoriously labour intensive but this approach may well be inescapable.
机译:导致肺部损伤的许多血源性异源生物并非天生具有中毒作用,而是在代谢激活后引起靶细胞内的损伤。这种损伤通常局限于能够生物激活的细胞,因此,除了其临床意义外,它还提供了肺中众多细胞类型内正常代谢活性的重要指标。毫不奇怪,损伤不仅仅反映特定酶的存在或不存在,而是反映活化和失活机制之间的平衡。不同酶之间平衡的变化也可能决定激活是导致损伤还是肿瘤发生(Foster等,1992)。无法通过分析整个肺匀浆来确定特定类型细胞的变化。特定细胞类型的分离可以提供有价值的信息,但是这种方法不能解决相同类型相邻细胞之间的差异(Forkert&Moussa 1989; Dinsdale等人1992)。进一步的进展可能需要将损伤与单个细胞的状态联系起来。组织化学和免疫细胞化学数据的定量化是费力的,但是这种方法可能是不可避免的。

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