Oxidative damage induced by carcinogenic polycyclic aromatic hydrocarbons and organic extracts from urban air particulate matter
Oxidative damage induced by carcinogenic polycyclic aromatic hydrocarbons and organic extracts from urban air particulate matter
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DOI：
10.1016/j.mrgentox.2009.12.018
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发表时间：
2010-02-02
影响因子：
1.9
通讯作者：
Sram, Radim J.
中科院分区：
文献类型：
--
作者：
Hanzalova, Katerina;Rossner, Pavel, Jr.;Sram, Radim J.
我们研究了氧化损伤在选定的单个致癌多环芳烃（c-PAH：苯并[a]芘，B[a]P;二苯并[a，l]芘，DB[a，l]P）、c-PAH人工混合物（c-PAH mix）和城市空气颗粒物（PM）中可提取有机物（EOM）的作用机制中的作用。用各种浓度的化合物和混合物处理两种细胞系（人肝癌细胞，HepG 2;人二倍体肺成纤维细胞，HEL）24和48小时。一组氧化应激标志物包括8-氧代脱氧鸟苷（8-oxodG）、15-F-2 t-IsoP和蛋白质羰基。细胞系对测试化合物的响应是显著不同的。在HepG 2细胞中，对DNA的氧化损伤通常不被单独的c-PAH和c-PAH混合物诱导，但EOM增加了这些细胞中的8-oxodG水平。在HEL细胞中，没有化合物诱导氧化DNA损伤。脂质过氧化反应，以15-F-2 t-lsoP的水平来衡量，c-PAHs在HepG 2细胞中仅在孵育48 h后才诱导，而EOM的作用在24 h后就已检测到。在HEL细胞中，单个c-PAH和c-PAH混合物通常降低15-F-2 t-lsoP水平。这种效果对于EOM治疗甚至更强。在任一细胞系中，用任何化合物处理24小时后，均未诱导蛋白质氧化（评估为细胞裂解物中的羰基水平）。处理48小时后，除DB[a，l]P在HepG 2细胞中外，单独的c-PAH和c-PAH混合物通常诱导两种细胞系中的蛋白质氧化。孵育48 h后，在HepG 2细胞中，由EOM引起的蛋白质氧化损伤普遍增加，而在HEL细胞中，仅观察到一个剂量的EOM的效果。总之，我们的研究结果表明，EOM的能力，诱导DNA和脂质的氧化损伤后24小时的处理，并在48小时后，在HepG 2细胞的蛋白质，而c-PAH的影响是实质上less. The诱导的氧化应激c-PAH和EOM在HEL细胞是弱的。(C)2010爱思唯尔有限公司版权所有。
We investigated the role of oxidative damage in the mechanism of action of selected individual carcinogenic PAHs (c-PAHs: benzo[a]pyrene, B[a]P; dibenzo[a,l]pyrene, DB[a,l]P), an artificial mixture of c-PAHs (c-PAHs mix) and extractable organic matter (EOM) from urban air particulate matter (PM). Two cell lines (human hepatoma cells, HepG2; human diploid lung fibroblasts, HEL) were treated for 24 and 48h with various concentrations of compounds and mixtures. A panel of oxidative stress markers included 8-oxodeoxyguanosine (8-oxodG), 15-F-2t-isoprostane (15-F-2t-IsoP) and protein carbonyl groups. The response of the cell lines to the test compounds was substantially different. In HepG2 cells, oxidative damage to DNA was generally not induced by individual c-PAHs and the c-PAHs mix, but EOM increased 8-oxodG levels in these cells. In HEL cells, none of the compounds induced oxidative DNA damage. Lipid peroxidation, measured as the level of 15-F-2t-lsoP, was induced by c-PAHs in HepG2 cells only after 48 h of incubation, while the effect of EOM was detected already after 24 h. In HEL cells, individual c-PAHs and the c-PAH mix generally decreased 15-F-2t-lsoP levels. This effect was even stronger for EOM treatment. Protein oxidation, assessed as carbonyl levels in cell lysates, was not induced after 24h of treatment with any compound in either cell line. Individual c-PAHs and the c-PAH mix generally induced protein oxidation in both cell lines after 48 h treatment, with the exception of DB[a,l]P in HepG2 cells. Oxidative damage to proteins caused by EOM was generally increased in HepG2 cells after 48 h of incubation, while in HEL cells the effect was observed for only one dose of EOM. In summary, our results demonstrate the ability of EOM to induce oxidative damage to DNA and lipids after 24 h of treatment, and to proteins after 48 h, in HepG2 cells, while the effect of c-PAHs was substantially less. The induction of oxidative stress by c-PAHs and EOM in HEL cells was weak. (C) 2010 Elsevier B.V. All rights reserved.