Chemical toxicology of reactive species in the atmosphere: two decades of progress in an electron acceptor and an electrophile.
Chemical toxicology of reactive species in the atmosphere: two decades of progress in an electron acceptor and an electrophile.
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DOI：
10.2131/jts.41.sp37
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发表时间：
2016-01-01
期刊：
影响因子：
--
通讯作者：
Cong, Nho Luong
中科院分区：
文献类型：
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作者：
Kumagai, Yoshito;Abiko, Yumi;Cong, Nho Luong
人们认为，柴油废气颗粒（DEP）等空气污染物会导致肺部疾病，如哮喘，这是氧化应激的结果。虽然DEP含有大量的多环芳烃，但我们主要关注9,10-菲醌（9,10- pq）和1,2-萘醌（1,2- nq），因为它们的化学性质基于它们的氧化和化学修饰能力。我们发现9,10- pq与NADPH（在酶的存在下）和二硫醇等电子供体相互作用，通过氧化还原循环产生过量的活性氧（ROS）。我们还发现1,2- nq能够修饰蛋白质硫醇，导致蛋白质加合物在较低浓度下激活氧化还原信号转导途径，而在较高浓度下产生毒性。在这篇综述中，我们简要介绍了我们近二十年来的发现。
Air pollutants such as diesel exhaust particles (DEP) are thought to cause pulmonary diseases such as asthma as a result of oxidative stress. While DEP contain a large number of polycyclic aromatic hydrocarbons, we have focused on 9,10-phenanthrenequinone (9,10-PQ) and 1,2-naphthoquinone (1,2-NQ) because of their chemical properties based on their oxidative and chemical modification capabilities. We have found that 9,10-PQ interacts with electron donors such as NADPH (in the presence of enzymes) and dithiols, resulting in generation of excess reactive oxygen species (ROS) through redox cycling. We have also shown that 1,2-NQ is able to modify protein thiols, leading to protein adducts associated with activation of redox signal transduction pathways at lower concentrations and toxicity at higher concentrations. In this review, we briefly introduce our findings from the last two decades.