大气颗粒物致机体损伤的OH自由基机制  

Hydroxyl Radical Mechanism of Toxicity Induced by Atmospheric Particulate Matter

作　　者：李怡[1] 朱彤[1] 

机构地区：[1]北京大学环境学院环境模拟与污染控制国家联合重点实验室,北京100871

出　　处：《生态毒理学报》2007年第2期142-149,共8页Asian Journal of Ecotoxicology

基　　金：国家重点基础研究发展规划(973)项目(No.2002CB410802);国家自然科学基金项目(No.20637020)

摘　　要：流行病学研究表明可吸入大气颗粒物浓度上升与人群呼吸道和心血管疾病发病率上升密切相关.毒理学实验和人体暴露研究显示可吸入大气颗粒物可导致机体广泛的损伤,但其致毒机制尚未明确.大量体内和体外研究表明了活性氧在颗粒物致毒过程中的重要作用,其中OH自由基具有极高的反应活性,是可吸入颗粒物致毒的重要机制.在总结国内外相关研究基础上,综述了OH自由基可能造成的大分子损伤、大气可吸入颗粒物暴露引发机体产生OH自由基的分子机制以及生物体系中OH自由基的检测手段,并对该领域的研究方向进行了展望.Epidemiological studies show that exposure to increased levels of particulate matter is strongly and consistently associated with increased cardiopulmonary morbidity and mortality. Toxicological and clinical studies also demonstrate that PM can cause vast damages to human body. PMt0 is a mixture of inorganic and organic components that varies in size, origin, and composition. Mechanisms under the health effects are still poorly understood. In vivo and in vitro studies suggest an important role of reactive oxygen species （ROS） in the mechanism of toxicity. Among the ROS, hydroxyl radical （·OH） is the most reactive and its generation is the key step of the toxicological mechanism. The pro-inflammatory effects of ROS, the damage to the biomolecules caused by＂ OH, the molecular mechanism of its generation and the detection methods are discussed in this paper.

关 键 词：大气颗粒物 OH自由基 致毒机制 

分 类 号：X513[环境科学与工程—环境工程]