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Influence of nutrition in PCB-induced vascular inflammation
Authors:Michael C Petriello  Bradley Newsome  Bernhard Hennig
Institution:1. Graduate Center for Toxicology, University of Kentucky, Lexington, KY, 40536-0200, USA
3. SRP Center, University of Kentucky, Room 599, Wethington Building, 900 South Limestone Street, Lexington, KY, 40536-0200, USA
2. Department of Chemistry, University of Kentucky, Lexington, KY, 40506-0055, USA
Abstract:The nutritional profile of an individual can influence the toxicity of persistent environmental toxicants. Polychlorinated biphenyls (PCBs), prevalent environmental pollutants, are highly lipid-soluble toxic compounds that biomagnify through trophic levels and pose cancer, neurocognitive, and atherosclerotic risk to human populations. There is a growing body of knowledge that PCBs can initiate inflammatory responses in vivo, and this inflammation can be either exacerbated or ameliorated by nutrition. Data indicate that diets high in certain dietary lipids such as omega-6 fatty acids can worsen PCB-induced vascular toxicity while diets enriched with bioactive food components such as polyphenols and omega-3 polyunsaturated fatty acids can improve the toxicant-induced inflammation. There is evidence that bioactive nutrients protect through multiple cell signaling pathways, but we have shown that lipid raft caveolae and the antioxidant defense controller nuclear factor (erythroid-derived 2)-like 2 (Nrf2) both play a predominant role in nutritional modulation of PCB-induced vascular toxicity. Interestingly, there appears to be an intimate cross-talk between caveolae-related proteins and cellular Nrf2, and focusing on the use of specific bioactive food components that simultaneously alter both pathways may produce a more effective and efficient cytoprotective response to toxicant exposure. The use of nutrition as a protective tool is an economically beneficial means to address the toxicity of persistent environmental toxicants and may become a sensible means to protect human populations from PCB-induced vascular inflammation and associated chronic diseases.
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