TOXIC INTERACTIONS OF AIR POLLUTANT COMPOUNDS

空气污染物的毒性相互作用

• 批准号: 7381500
• 负责人: MICHAEL P DOHM
• 金额: $ 14.19万
• 依托单位: UNIVERSITY OF HAWAII AT MANOA
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-05-01 至 2007-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7381500
• 关键词: TOXIC; INTERACTIONS; AIR; POLLUTANT; COMPOUNDS

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Mammalian macrophages are known to produce reactive oxygen species during phagocytosis or stimulation by a variety of agents including ozone and aerosol sulfates. Superoxide anion and hydrogen peroxide are produced in aerobic cells either as a by-product during mitochondrial respiration or by oxidoreductases. The respiratory burst is performed by activation of NADPH oxidase and is believed to be crucial for the bactericidal action of phagocytes. Ozone exposure generally leads to respiratory burst from macrophages, and also reduction in anitoxidant activities of epithelial cells, providing one mechanism for inflammation to lung tissue. ROS and the antioxidant system has been investigated in frogs, but has not been studied in light of the innate immunity and the pulmonary system of any amphibian. This study will examine the immune defense responses to ozone and acidic sulfate aerosols in vitro exposures to toad (Bufo marinus) phagocytes. The investigator will (1) create an exposure system using viable cascade impactors to perform exposures of cells in culture, (2) establish cell culturing capability at Chaminade University, and (3) identify ROS released by amphibian macrophages. The primary objective of the work will be to establish whether ozone and or SO2 aerosols activate or suppress functional capacities of amphibian macrophages, particularly in relation to the respiratory burst and the effects on antioxidant enzymes present in the lung and whether these patterns are similar to results typical of mammalian models. Future efforts will be directed at investigating redundancy of the cytokine effects, particularly tumor necrosis factor ? alpha, leading to inflammation in non-mammalian vertebrates using amphibian macrophages as a model system.

该子项目是利用NIH/NCRR资助的中心赠款提供的资源的许多研究子项目之一。子弹和调查员（PI）可能已经从其他NIH来源获得了主要资金，因此可以在其他清晰的条目中代表。列出的机构适用于该中心，这不一定是调查员的机构。已知哺乳动物巨噬细胞在吞噬或刺激（包括臭氧和气溶胶硫酸盐）刺激期间产生活性氧。超氧化物阴离子和过氧化氢是在有氧细胞中作为线粒体呼吸过程中的副产品或氧化酶的副产品产生的。呼吸爆发是通过激活NADPH氧化酶进行的，据信对于吞噬细胞的杀菌作用至关重要。臭氧暴露通常会导致巨噬细胞的呼吸道爆发，并减少上皮细胞的氧化活性，从而为肺组织提供了一种炎症机制。 ROS和抗氧化剂系统已在青蛙中进行了研究，但尚未根据任何两栖动物的先天免疫力和肺系统进行研究。这项研究将检查对蟾蜍对蟾蜍（Bufo Marinus）吞噬细胞的体外暴露于臭氧和酸性硫酸盐气溶胶的免疫防御反应。研究者（1）使用可行的级联撞击器创建一个暴露系统，以在培养中进行细胞的暴露，（2）在夏尼纳大学建立细胞培养能力，（3）确定两栖动物巨噬细胞释放的ROS。这项工作的主要目的是确定臭氧和或SO2气溶胶是否激活或抑制两栖动物巨噬细胞的功能能力，尤其是与呼吸爆发以及对肺中存在的抗氧化酶的影响以及这些模式是否与哺乳动物模型的典型结果相似。未来的努力将致力于研究细胞因子作用的冗余，尤其是肿瘤坏死因子？ α，导致使用两栖巨噬细胞作为模型系统的非哺乳动物脊椎动物的炎症。