University of Kentucky SRP Center, University of Kentucky, Lexington, KY, 40536-0200, USA.
Environ Sci Pollut Res Int. 2014 May;21(10):6354-64. doi: 10.1007/s11356-013-1591-3. Epub 2013 Mar 16.
Persistent organic pollutants such as polychlorinated biphenyls (PCBs) are associated with detrimental health outcomes including cardiovascular diseases. Remediation of these compounds is a critical component of environmental policy. Although remediation efforts aim to completely remove toxicants, little is known about the effects of potential remediation byproducts. We previously published that Fe/Pd nanoparticles effectively dechlorinate PCB 77 to biphenyl, thus eliminating PCB-induced endothelial dysfunction using primary vascular endothelial cells. Herein, we analyzed the toxic effects of PCB congener mixtures (representative mixtures of commercial PCBs based on previous dechlorination data) produced at multiple time points during the dechlorination of PCB 77 to biphenyl. Compared with pure PCB 77, exposing endothelial cells to lower chlorinated PCB byproducts led to improved cellular viability, decreased superoxide production, and decreased nuclear factor kappa B activation based on duration of remediation. Presence of the parent compound, PCB 77, led to significant increases in mRNA and protein inflammatory marker expression. These data implicate that PCB dechlorination reduces biological toxicity to vascular endothelial cells.
持久性有机污染物，如多氯联苯（PCBs），与心血管疾病等有害健康后果有关。这些化合物的修复是环境政策的一个关键组成部分。尽管修复工作旨在完全去除有毒物质，但对于潜在修复副产物的影响知之甚少。我们之前发表过，Fe/Pd 纳米粒子可有效地将 PCB 77 脱氯为联苯，从而使用原代血管内皮细胞消除 PCB 引起的内皮功能障碍。在此，我们分析了在将 PCB 77 脱氯为联苯的过程中，在多个时间点生成的 PCB 同系物混合物（基于先前脱氯数据的商业 PCB 代表性混合物）的毒性影响。与纯 PCB 77 相比，暴露于低氯化 PCB 副产物的内皮细胞的细胞活力提高，超氧化物产生减少，核因子 kappa B 激活减少，这取决于修复时间的长短。母体化合物 PCB 77 的存在导致 mRNA 和蛋白质炎症标志物的表达显著增加。这些数据表明 PCB 脱氯可降低对血管内皮细胞的生物毒性。
