Air pollution is one of the major environmental risks threatening human health, diesel exhaust particulate matter (DEPM) is an important source of urban air pollution, and oral ingestion is the primary route of exposure to atmospheric particulate matter. This study examined the bioaccessibility of Cr, Fe, and Zn in DEPM within simulated saliva fluids through in vitro experiments, interactions between the particles and mucins, and the mechanisms underlying the oxidative damage they cause. The results indicated that the interaction between DEPM and mucins altered the dispersibility, surface charge, and wettability of the particles, leading to increased release of heavy metals. Protein adsorption experiments and characterizations revealed that the adsorption of mucin by the particles resulted in a complexation reaction between the metals in the DEPM and the mucins, accompanied by fluorescence quenching of the protein. In addition, free radical assays and correlation analyses revealed that environmentally persistent free radicals generated by DEPM induce the production of reactive oxygen species (O2·−, HOOH, and·OH), which damage the secondary structure of mucins and increase the risk of oral diseases. Our study is the first to reveal the interaction between DEPM and mucins in saliva, elucidating the mechanisms of DEPM-induced oxidative damage. This is significant for understanding the oral health risks posed by the ingestion of atmospheric particulate matter.

中文翻译：

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模拟唾液中柴油机尾气颗粒物与粘蛋白的相互作用：重金属的生物可及性和潜在的健康风险


空气污染是威胁人类健康的主要环境风险之一，柴油机尾气颗粒物 （DEPM） 是城市空气污染的重要来源，经口摄入是接触大气颗粒物的主要途径。本研究通过体外实验、颗粒与粘蛋白之间的相互作用以及它们引起的氧化损伤的潜在机制，检查了模拟唾液中 DEPM 中 Cr、Fe 和 Zn 的生物可及性。结果表明，DEPM 和粘蛋白之间的相互作用改变了颗粒的分散性、表面电荷和润湿性，导致重金属的释放增加。蛋白质吸附实验和表征表明，颗粒对粘蛋白的吸附导致 DEPM 中的金属与粘蛋白之间发生络合反应，并伴有蛋白质的荧光猝灭。此外，自由基测定和相关分析表明，DEPM 产生的环境持久性自由基诱导活性氧（O2·−、HOOH 和·OH），这会破坏粘蛋白的二级结构并增加患口腔疾病的风险。我们的研究首次揭示了 DEPM 与唾液中粘蛋白之间的相互作用，阐明了 DEPM 诱导的氧化损伤的机制。这对于了解摄入大气颗粒物带来的口腔健康风险非常重要。