摘要
大气颗粒物(PM)是大气中各种具有不同化学组分的颗粒状物质的混合体。其中,空气动力学直径≤10μm和≤2.5μm的可吸入颗粒物(PM10和PM2.5)由于吸附有重金属、多环芳烃等有机物及细菌、病毒等有害成分,并能够通过呼吸系统进入体内,因此对人体健康具有极大的危害作用。流行病学研究数据显示,大气中PM含量增加会显著提高呼吸道和心血管疾病的发病率和致死率。因此,揭示PM诱导呼吸系统和心血管系统损伤的分子机制,对于制定相应防治策略、减低环境相关疾病的危害具有重要意义和医学价值。我们根据目前有限的研究线索,对PM诱导细胞损伤反应中涉及的氧化应激、内质网应激和炎性反应等机制做一综述。
Ambient particulate matter（PM） is a complex mixture of the particles with different chemical composition. The coarse and fine fraction of PM, which are smaller than 10 μm and 2.5 μm in diameter（PM10 and PM2.5）, have been shown to be the most important hazardous components for mediating PM toxicity due to the adsorbed elements（such as heavy metals, organic components including PAH, etc） to their surface. Data from the epidemiological studies have associated the increasing PM concentration with more incidence and mortality of the cardiopulmonary disorders. Therefore, understanding the molecular mechanism of PM-induced toxicity in the pulmonary and cardiovascular system will be helpful for finding the effective strategies to evade the injury induced by PM. Here we have summarized the recent data regarding the mechanisms for mediating PM cytotoxical effects by inducing oxidative stress, inflammation and the endoplasmic reticulumn stress.
出处
《生物技术通讯》
CAS
2012年第4期617-620,共4页
Letters in Biotechnology
基金
国家自然科学基金(30871277
30970594
31172342)
国家重点基础研究发展计划(2011CB503803)
北京市自然科学基金(5092022
5102035)
关键词
大气颗粒物
氧化应激
内质网应激
炎性反应
particulate matter
oxidative stress
inflammation
endoplasmic reticulumn stress
