TOXIC INTERACTIONS OF AIR POLLUTANT COMPOUNDS

空气污染物的毒性相互作用

• 批准号: 7610127
• 负责人: MICHAEL P DOHM
• 金额: $ 16.78万
• 依托单位: UNIVERSITY OF HAWAII AT MANOA
• 依托单位国家: 美国
• 财政年份: 2007
• 资助国家: 美国
• 起止时间: 2007-05-01 至 2008-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7610127
• 关键词: Acute; Adult; Affect; Air Pollutants; Air Pollution; Alveolar Macrophages; Cardiovascular Diseases; Cell Surface Proteins; Complex; Computer Retrieval of Information on Scientific Projects Database; Coronary; Environmental Pollutants; Epidemiologic Studies; Epithelial Cells; Event; Funding; Gene Expression Regulation; Generations; Genetic; Grant; Health; Human; Institution; Irritants; Link; Lipids; Lung; Microarray Analysis; Molecular; Ozone; Pattern; Population; Reactive Oxygen Species; Research; Research Personnel; Resources; Rodent Model; Signal Transduction; Smog; Source; United States National Institutes of Health; aged; cell type; chemokine; cytokine; middle age; Acute; Adult; Affect; Air Pollutants; Air Pollution; Alveolar Macrophages; Cardiovascular Diseases; Cell Surface Proteins; Complex; Computer Retrieval of Information on Scientific Projects Database; Coronary; Environmental Pollutants; Epidemiologic Studies; Epithelial Cells; Event; Funding; Gene Expression Regulation; Generations; Genetic; Grant; Health; Human; Institution; Irritants; Link; Lipids; Lung; Microarray Analysis; Molecular; Ozone; Pattern; Population; Reactive Oxygen Species; Research; Research Personnel; Resources; Rodent Model; Signal Transduction; Smog; Source; United States National Institutes of Health; aged; cell type; chemokine; cytokine; middle age

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. Ozone (O3) is a major constituent of photochemical smog, and continues to be a significant component of urban air pollution. Ozone is a strong pulmonary irritant, and it induces its adverse affects by acting directly with cell surface proteins and lipids, or indirectly via reactive oxygen species (ROS) generation which leads to oxidative damage. Epidemiological studies link O3 to adverse health effects in humans, particularly among sensitive populations (aged, young, asthmatics), but O3-exposure is also associated with acute coronary events in otherwise healthy, middle-aged adults. In rodent models, the effects of O3 are strain-specific, suggesting genetic background is significant. Most studies also implicate modulation by cytokines/chemokines signaling among different cell types (resident macrophages, alveolar epithelial cells, etc.). Thus, studies seeking to elucidate how environmental pollutants alter or even trigger molecular mechanisms that contribute to cardiovascular disease may require multifactorial approaches. Current microarray technology provides such an approach, permitting analysis of complex gene expression and regulation patterns between experimental and control subjects.

该副本是利用众多研究子项目之一 由NIH/NCRR资助的中心赠款提供的资源。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。列出的机构是 对于中心，这不一定是调查员的机构。 臭氧（O3）是光化学烟雾的主要组成部分，并且仍然是城市空气污染的重要组成部分。臭氧是一种强烈的肺部刺激性，它通过直接与细胞表面蛋白和脂质作用，或通过活性氧（ROS）产生间接引起其不良影响，从而导致氧化损伤。流行病学研究将O3与人类的不良健康影响联系起来，尤其是在敏感人群（年龄，年轻，哮喘患者中），但O3暴露也与其他健康的中年成年人中的急性冠状动脉事件有关。在啮齿动物模型中，O3的作用是特异性的，表明遗传背景很重要。大多数研究还暗示了不同细胞类型（驻留巨噬细胞，肺泡上皮细胞等）中细胞因子/趋化因子信号传导的调节。因此，旨在阐明环境污染物如何改变甚至触发导致心血管疾病的分子机制的研究可能需要多因素方法。当前的微阵列技术提供了这种方法，可以分析实验和对照对象之间的复杂基因表达和调节模式。