These hypotheses will be tested in vitro as well as in vivo by studying the interactions of PCBs with dietary compounds such as fatty acids and antioxidants. Importantly, we will use cell and mouse models lacking the caveolin gene to determine the involvement of caveolae in the PCB and fatty acid uptake and toxicity. We propose to explore mechanisms of nutrient-mediated modulation of PCB toxicity, and the outcome of our proposed study may lead to novel nutritional recommendations and therapeutic interventions in populations exposed to Superfund chemicals.

PROJECT POSTERS AND PRESENTATIONS

• Activation of Peroxisome Proliferator Activated Receptors (PPAR) Is Altered by Exposure to Co-Planar 3, 3', 4, 4' Tetrachlorobiphenyl (PCB77)
• Alumina Nanoparticles Induce Endothelial Cell Dysfunction: Implications in Vascular Disease
• Benzo[a]pyerne-Induced Vascular Endothelial Adhesion Molecule Expression Can Be Disrupted by Selective Flavonoid Treatment
• Caveolae Mediate Pro-Inflammatory Properties of Coplanar Polychlorinated Biphenyls
• Caveolin-1 Mediates Up-Regulation of Pro-Inflammatory Cytokines by 3,4, 3', 4'-tetrachlorobiphenyl (PCB77)
• Dietary Flavonoids Block PCB-Induced Proinflammatory Responses in Vascular Endothelial Cells
• Endothelial Cell Caveolae Are Involved in Activation of Aryl Hydrocarbon Receptor Pathway by Coplanar Polychlorinated Biphenyls
• Nutritional Intervention to Modify Pro-atherogenic Effects of Persistent Organic Pollutants
• PPARa Agonists Protect Against PCB-Induced Vascular Endothelial Cell Activation
• Role of Caveolin-1 in EGCG-Mediated Protection Against Linoleic Acid-Induced Endothelial Cell Activation