College of Environment and Resource, Center of Environmental Science and Engineering, Shanxi University, Taiyuan, Shanxi, PR China.
Chemosphere. 2011 Mar;82(11):1589-96. doi: 10.1016/j.chemosphere.2010.11.055. Epub 2010 Dec 18.
Epidemiological studies suggest that NO₂ inhalation is associated with adverse effects on heart-related health, however, existing experimental data lack relevant evidences. In this study, a role for oxidative stress, endothelial dysfunction and inflammatory responses in the heart of rats treated with different concentrations of NO₂ (0, 5, 10 and 20 mg m⁻³) was investigated. Mild heart pathology occurred after 7-d exposure (6 h d⁻¹). Marked oxidative stress were induced as evaluated by reduction/induction of antioxidants (Cu/Zn-SOD, Mn-SOD and GPx) activity and increasing formation of MDA and PCO. Also, mRNA and protein biomarkers of vasoconstriction (ET-1, eNOS) and inflammation (TNF-α, IL-1β and ICAM-1) were up-regulated, and p53 mRNA expression, bax/bcl-2 ratio and the mean number of TUNEL-positive myocytes were increased as well. All the results implicate that NO₂ exerted injuries to mammals' heart, and the damage mechanisms were possibly associated with oxidative stress, endothelial dysfunction and inflammation.
流行病学研究表明，NO₂吸入与心脏相关健康的不良影响有关，但现有实验数据缺乏相关证据。在这项研究中，研究了不同浓度的 NO₂（0、5、10 和 20 mg m⁻³）对大鼠心脏的氧化应激、内皮功能障碍和炎症反应的作用。7 天暴露（6 h d⁻¹）后出现轻度心脏病理学。通过减少/诱导抗氧化剂（Cu/Zn-SOD、Mn-SOD 和 GPx）活性以及增加 MDA 和 PCO 的形成来评估明显的氧化应激。此外，血管收缩（ET-1、eNOS）和炎症（TNF-α、IL-1β 和 ICAM-1）的 mRNA 和蛋白质生物标志物上调，p53 mRNA 表达、bax/bcl-2 比值和 TUNEL 阳性肌细胞的平均数量也增加。所有这些结果表明，NO₂对哺乳动物的心脏造成了伤害，其损伤机制可能与氧化应激、内皮功能障碍和炎症有关。
