Pryor W A, Squadrito G L, Friedman M
Biodynamics Institute, Louisiana State University, Baton Rouge, USA.
Free Radic Biol Med. 1995 Dec;19(6):935-41. doi: 10.1016/0891-5849(95)02033-7.
Ozone is so reactive that it can be predicted to be entirely consumed as it passes through the first layer of tissue it contacts at the lung/air interface. This layer includes the lung lining fluid (tracheobronchial surface fluid and alveolar and small airway lining fluid) and, where the lung lining fluid is thin or absent, the membranes of the epithelial cells that line the airways. Therefore, the biochemical changes that follow the inhalation of ozone must be relayed into deeper tissue strat by a cascade of ozonation products. Lipid ozonation products (LOP) are suggested to be the most likely species to act as signal transduction molecules. This is because unsaturated fatty acids are present in the lipids in both the lung lining fluid and in pulmonary cell bilayers, and ozone reacts with unsaturated fatty acids to produce ozone-specific products. Further, lipid ozonation products are finite in number, have structures that are predictable from the Criegee ozonation mechanism, and are small, diffusible, stable (or metastable) molecules. Preliminary data show that individual LOP cause the activation of specific lipases, which trigger the release of endogenous mediators of inflammation.
臭氧具有很强的反应活性，因此可以预测，当它通过肺/空气界面处接触到的第一层组织时会被完全消耗。这一层包括肺内膜液（气管支气管表面液、肺泡和小气道内膜液），以及在肺内膜液稀薄或不存在的地方，气道内衬上皮细胞的膜。因此，吸入臭氧后发生的生化变化必须通过一系列臭氧化产物传递到更深层的组织中。脂质臭氧化产物（LOP）被认为是最有可能作为信号转导分子的物质。这是因为不饱和脂肪酸存在于肺内膜液和肺细胞双层膜的脂质中，臭氧与不饱和脂肪酸反应会产生特定于臭氧的产物。此外，脂质臭氧化产物数量有限，具有可根据克里格臭氧化机制预测的结构，并且是小的、可扩散的、稳定（或亚稳定）的分子。初步数据表明，单个LOP会导致特定脂肪酶的激活，从而引发内源性炎症介质的释放。
