Laboratory of Genetic Ecotoxicology, Institute of Experimental Medicine AS CR, Videnska 1083, 142 20 Prague, Czech Republic.
Mutat Res. 2011 Aug 1;713(1-2):76-82. doi: 10.1016/j.mrfmmm.2011.06.001. Epub 2011 Jun 12.
Air pollution causes oxidative damage to macromolecules, chromosomal aberrations and changes in gene expression. We investigated the levels of oxidative stress markers [8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG), 15-F(2t)-isoprostane (15-F2t-IsoP), protein carbonyls] and cytogenetic parameters [genomic frequency of translocations (F(G)/100), percentage of aberrant cells (%AB.C.) and acentric fragments (ace)] in subjects living in Prague and in the heavily polluted Ostrava region. We also compared the expression of genes participating in base excision repair (BER) and non-homologous end-joining (NHEJ). We analyzed 64 subjects from Prague and 75 subjects from Ostrava. We measured oxidative stress markers by ELISA, cytogenetic parameters by fluorescence in situ hybridization and gene expression by quantitative PCR. The levels of air pollutants (benzo[a]pyrene, B[a]P; carcinogenic polycyclic aromatic hydrocarbons, c-PAHs; benzene) measured by personal monitors were significantly elevated in Ostrava compared to Prague (p<0.001). Despite this fact, we observed no differences in biomarkers of oxidative stress between the two locations. Moreover, subjects from Ostrava were less likely to have above-median levels of %AB.C. (OR; 95% CI: 0.18; 0.05-0.67; p=0.010). Multivariate analyses revealed that subjects living in Ostrava had increased odds of having above-median levels of XRCC5 expression (OR; 95% CI: 3.33; 1.03-10.8; q=0.046). Above-median levels of 8-oxodG were associated with decreased levels of vitamins C (OR; 95% CI: 0.37; 0.16-0.83; p=0.016) and E (OR; 95% CI: 0.25; 0.08-0.75; p=0.013), which were elevated in subjects from Ostrava. We suggest that air pollution by c-PAHs affects XRCC5 gene expression, which probably protects subjects from Ostrava against the induction of a higher frequency of translocations; elevated vitamin C and E levels in the Ostrava subjects decrease the levels of 8-oxodG.
空气污染导致大分子氧化损伤、染色体畸变和基因表达改变。我们研究了生活在布拉格和污染严重的俄斯特拉发地区的人群中氧化应激标志物[8-氧-7,8-二氢-2'-脱氧鸟苷（8-氧-dG）、15-F（2t）-异前列腺素（15-F2t-IsoP）、蛋白质羰基]和细胞遗传学参数[基因组易位频率（F（G）/100）、异常细胞百分比（%AB.C.）和无着丝粒片段（ace）]的水平。我们还比较了参与碱基切除修复（BER）和非同源末端连接（NHEJ）的基因表达。我们分析了来自布拉格的 64 名受试者和来自俄斯特拉发的 75 名受试者。我们通过 ELISA 测量氧化应激标志物，通过荧光原位杂交测量细胞遗传学参数，通过定量 PCR 测量基因表达。通过个人监测器测量的空气污染物（苯并[a]芘，B[a]P；致癌多环芳烃，c-PAHs；苯）的水平在俄斯特拉发明显高于布拉格（p<0.001）。尽管如此，我们在两个地点之间没有观察到氧化应激生物标志物的差异。此外，来自俄斯特拉发的受试者%AB.C.中位数以上水平的可能性较低（OR；95%CI：0.18；0.05-0.67；p=0.010）。多变量分析显示，居住在俄斯特拉发的受试者 XRCC5 表达中位数以上水平的几率增加（OR；95%CI：3.33；1.03-10.8；q=0.046）。8-氧-dG 中位数以上水平与维生素 C（OR；95%CI：0.37；0.16-0.83；p=0.016）和维生素 E（OR；95%CI：0.25；0.08-0.75；p=0.013）水平降低有关，而俄斯特拉发受试者的维生素 C 和 E 水平升高。我们认为，c-PAHs 造成的空气污染会影响 XRCC5 基因表达，这可能会保护俄斯特拉发的受试者免受更高频率易位的诱导；俄斯特拉发受试者中维生素 C 和 E 水平升高会降低 8-氧-dG 水平。
