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首页> 外文期刊>Archives of Toxicology >Effects of asphalt fume condensate exposure on acute pulmonary responses.
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Effects of asphalt fume condensate exposure on acute pulmonary responses.

机译：暴露于沥青烟气冷凝物对急性肺反应的影响。

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OBJECTIVE: The present study was carried out to characterize the effects of in vitro exposure to paving asphalt fume condensate (AFC) on alveolar macrophage (AM) functions and to monitor acute pulmonary responses to in vivo AFC exposure in rats. METHODS: For in vitro studies, rat primary AM cultures were incubated with various concentrations of AFC for 24 h at 37 degrees C. AM-conditioned medium was collected and assayed for lactate dehydrogenase (LDH) as a marker of cytotoxicity. Tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 (IL-1) production were assayed in AM-conditioned medium to monitor AM function. The effect of AFC on chemiluminescence (CL) generated by resting AM or AM in response to zymosan or PMA stimulation was also determined as a marker of AM activity. For in vivo studies, rats received either (1) a single intratracheal (IT) instillation of saline, or 0.1 mg or 0.5 mg AFC and were killed 1 or 3 days later; or (2) IT instillation of saline, or 0.1, 0.5, or 2 mg AFC for three consecutive days and were killed the following day. Differential counts of cells harvested by bronchoalveolar lavage were measured to monitor inflammation. Acellular LDH and protein content in the first lavage fluid were measured to monitor damage. CL generation, TNF-alpha and IL-1 production by AM were assayed to monitor AM function. RESULTS: In vitro AFC exposure at <200 microg/ml did not induce cytotoxicity, oxidant generation, or IL-1 production by AM, but it did cause a small but significant increase in TNF-alpha release from AM. In vitro exposure of AM to AFC resulted in a significant decline of CL in response to zymosan or PMA stimulation. The in vivo studies showed that AFC exposure did not induce significant neutrophil infiltration or alter LDH or protein content in acellular lavage samples. Macrophages obtained from AFC-exposed rats did not show significant differences in oxidant production or cytokine secretion at rest or in response to LPS in comparison with control macrophages. CONCLUSIONS: These results suggest that: (1) in vitro AFC exposure did not adversely affect cell viability or induce the release of high levels of inflammatory cytokines or oxidants; and (2) exposure of rats to AFC did not cause acute pulmonary inflammation or injury, and did not significantly alter AM functions.
机译：目的：本研究旨在表征体外暴露于铺路的沥青烟气冷凝物（AFC）对肺泡巨噬细胞（AM）功能的影响，并监测急性肺反应对大鼠体内AFC暴露的影响。方法：为了进行体外研究，将大鼠原代AM培养物与各种浓度的AFC在37摄氏度下孵育24小时。收集AM条件培养基，并测定乳酸脱氢酶（LDH）作为细胞毒性的标志。在AM条件培养基中检测肿瘤坏死因子-α（TNF-α）和白介素-1（IL-1）的产生，以监测AM功能。还确定了AFC对静止AM或AM响应酵母聚糖或PMA刺激而产生的化学发光（CL）的影响，作为AM活性的标志物。为了进行体内研究，大鼠接受（1）一次气管内（IT）盐水或0.1 mg或0.5 mg AFC滴注，并在1或3天后被杀死;或（2）连续三天IT滴注盐水，0.1、0.5或2 mg AFC，并于第二天杀死。测量通过支气管肺泡灌洗收获的细胞的差异计数以监测炎症。测量第一灌洗液中的脱细胞LDH和蛋白质含量以监测损伤。检测由AM产生的CL，TNF-α和IL-1，以监测AM的功能。结果：低于200 microg / ml的体外AFC暴露不会引起AM的细胞毒性，氧化剂生成或IL-1产生，但确实导致AM中的TNF-α释放量小而显着增加。 AM对AFC的体外暴露导致对酵母聚糖或PMA刺激的CL显着下降。体内研究表明，暴露于AFC不会引起明显的中性粒细胞浸润或改变脱细胞灌洗样品中的LDH或蛋白质含量。与对照组巨噬细胞相比，从暴露于AFC的大鼠中获得的巨噬细胞在静止或对LPS的反应中，氧化剂产生或细胞因子分泌没有显着差异。结论：这些结果表明：（1）体外AFC暴露不会对细胞活力产生不利影响或诱导高水平的炎性细胞因子或氧化剂释放。 （2）大鼠暴露于AFC不会引起急性肺部炎症或损伤，也不会显着改变AM功能。

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