Antognelli Cinzia, Gambelunghe Angela, Del Buono Chiara, Murgia Nicola, Talesa Vincenzo N, Muzi Giacomo
Department of Experimental Medicine, University of Perugia, via del Giochetto 06123, Perugia, Italy.
Chem Biol Interact. 2009 Nov 10;182(1):13-21. doi: 10.1016/j.cbi.2009.08.002. Epub 2009 Aug 11.
Reactive oxygen species (ROS) play an important role as mediators of pulmonary damage in mineral dust-induced diseases. Studies carried out to date have largely focused on silica-induced production of ROS by lung phagocytes. In this study we investigated the hypothesis that crystalline silica Min-U-Sil 5 can induce elevations in intracellular ROS in human bronchial epithelial cells BEAS-2B, via an indirect mechanism that involves ROS-inducing intracellular factors, through a reduction of antiglycation (glyoxalase enzymes) and antioxidant (paraoxonase 1 and glutathione-S-transferases) enzymatic defenses. The results show that crystalline silica Min-U-Sil 5 causes a significant reduction in the efficiency of antiglycation and antioxidant enzymatic defenses, paralleled by an early and extensive ROS generation, thus preventing the cells from an efficient scavenging action, and eliciting oxidative damage. These results confirm the importance of ROS in development of crystalline silica-induced oxidative stress and emphasize the pivotal role of antiglycation/antioxidant and detoxifying systems in determining the level of protection from free radicals-induced injury for cells exposed to crystalline silica Min-U-Sil 5.
活性氧（ROS）作为矿物粉尘诱导疾病中肺损伤的介质发挥着重要作用。迄今为止开展的研究主要集中在硅诱导肺吞噬细胞产生ROS。在本研究中，我们调查了以下假设：结晶二氧化硅Min-U-Sil 5可通过一种间接机制诱导人支气管上皮细胞BEAS-2B内的细胞内ROS升高，该机制涉及通过降低抗糖基化（乙二醛酶）和抗氧化（对氧磷酶1和谷胱甘肽-S-转移酶）酶防御来诱导ROS的细胞内因子。结果表明，结晶二氧化硅Min-U-Sil 5导致抗糖基化和抗氧化酶防御效率显著降低，同时伴有早期广泛的ROS生成，从而阻止细胞进行有效的清除作用，并引发氧化损伤。这些结果证实了ROS在结晶二氧化硅诱导的氧化应激发展中的重要性，并强调了抗糖基化/抗氧化和解毒系统在确定暴露于结晶二氧化硅Min-U-Sil 5的细胞免受自由基诱导损伤的保护水平方面的关键作用。
