Inhalation of common air pollutants such as diesel and biodiesel combustion products can induce vascular changes in humans which may contribute to increased mortality and morbidity associated with fine particulate matter exposures. Diesel, biodiesel, and other combustion byproducts contain fatty acid components capable of entering the body through particulate matter inhalation. Fatty acids can also be endogenously released into circulation following a systemic stress response to some inhaled pollutants such as ozone. When in the circulation, bioactive fatty acids may interact with cells lining the blood vessels, potentially inducing endothelial dysfunction. To examine whether fatty acids could potentially be involved in human vascular responses to air pollutants, we determined the effects of fatty acids and derivatives on important vascular cell functions. Human umbilical vein endothelial cells (HUVEC) were exposed in vitro to oleic acid (OA) or OA metabolites for 4-48 h. Cytotoxicity, vasodilator production (by ELISA measurement), mitochondrial function (using Sea Horse assays), and iron metabolism (inferred by ICP-OES measurements) were examined, with standard statistical testing (ANOVA, t-tests) employed. Dose-dependent cytotoxicity was noted at 24 h, with 12-hydroxy OA more potent than OA. Mitochondrial stress testing showed that 12-hydroxy OA and OA induce mitochondrial dysfunction. Analysis of soluble mediator release from HUVEC showed a dose-dependent increase in prostaglandin F2α, a lipid involved in control of vascular tone, at 24 h (85% above controls) after OA-BSA exposure. RT-PCR analysis revealed OA did not induce changes in gene expression at noncytotoxic concentrations in exposed HUVEC, but 12-OH OA did alter ICAM and COX2 gene expression. Together, these data demonstrate that FA may be capable of inducing cytotoxic effects and altering expression of mediators of vascular function following inhalation exposure, and may be implicated in air pollutant-induced deaths and hospitalizations. (267 of max 350 words).

中文翻译：

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油酸及其衍生物影响人内皮细胞线粒体功能和血管活性介质的产生。

吸入常见的空气污染物，例如柴油和生物柴油燃烧产物，会引起人体血管变化，这可能导致与细颗粒物暴露相关的死亡率和发病率增加。柴油，生物柴油和其他燃烧副产物包含脂肪酸成分，这些成分能够通过吸入颗粒物进入人体。在对某些吸入性污染物（例如臭氧）产生系统性应激反应后，脂肪酸也可以内源性释放到循环中。当处于循环中时，生物活性脂肪酸可能会与衬里血管的细胞相互作用，从而潜在地引起内皮功能障碍。为了检查脂肪酸是否可能参与人体对空气污染物的血管反应，我们确定了脂肪酸及其衍生物对重要血管细胞功能的影响。将人脐静脉内皮细胞（HUVEC）体外暴露于油酸（OA）或OA代谢产物中4-48小时。使用标准的统计检验（ANOVA，t检验），检查了细胞毒性，血管扩张剂的产生（通过ELISA测量），线粒体功能（使用Sea Horse分析）和铁代谢（通过ICP-OES测量推断）。在24小时时发现剂量依赖性细胞毒性，其中12-羟基OA比OA更有效。线粒体压力测试表明12-羟基OA和OA诱导线粒体功能障碍。从HUVEC释放的可溶性介体的分析表明，在OA-BSA暴露后24小时内，前列腺素F2α（与控制血管张力有关的脂质）呈剂量依赖性增加（比对照高85％）。RT-PCR分析显示，在暴露的HUVEC中，OA在无细胞毒性浓度下不会诱导基因表达的变化，但是12-OH OA确实会改变ICAM和COX2基因的表达。总之，这些数据表明，FA可能在吸入暴露后能够诱导细胞毒性作用并改变血管功能介质的表达，并且可能与空气污染物引起的死亡和住院有关。（最多350个字，共267个）。