PCB 77 dechlorination products modulate pro-inflammatory events in vascular endothelial cells |
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Authors: | Katryn Eske Bradley Newsome Sung Gu Han Margaret Murphy Dibakar Bhattacharyya Bernhard Hennig |
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Institution: | 1. University of Kentucky SRP Center, University of Kentucky, Lexington, KY, 40536-0200, USA 2. Graduate Center for Nutritional Sciences, University of Kentucky, Kentucky SRP Center, Room 599, Wethington Building, 900 South Limestone Street, Lexington, KY, 40536-0200, USA 3. Department of Chemistry, University of Kentucky, Lexington, KY, 40506-0055, USA 4. Department of Food Science of Animal Resources, College of Animal Bioscience and Technology, Konkuk University, Seoul, 143-701, Korea 5. Department of Chemical and Materials Engineering, University of Kentucky, Lexington, KY, 40506-0046, USA
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Abstract: | 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. |
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