Lei Wang received her Master’s of Science in Food Science and Nutrition from the China Agricultural University. Her thesis project was entitled "Effects of Omega-3 Polyunsaturated Fatty Acids on Calcium Metabolism in the Rat of Osteoporosis Model". In 2001, she presented her research data at the 17th International Congress of Nutrition held in Vienna, Austria, where she received the Young Investigator Bursary Award from the International Union of Nutritional Sciences Council.
Lei started working in the laboratory of Dr. Bernhard Hennig in the Graduate Center for Nutritional Sciences at the University of Kentucky in 2003. Her research focuses on the role of nutrients and toxins on biochemical and molecular mechanisms of vascular endothelial cell function, injury and protection by utilizing cell culture systems and in vivo animal models. Very little is known about the interaction of diets and cytotoxicity of Superfund contaminants like polychlorinated biphenyls (PCBs). Data from Dr. Hennig’s laboratory clearly show that nutrition can modulate PCB toxicity. For example, specific dietary fatty acids can amplify PCB toxicity in vascular endothelial cells, an event which can be blocked by antioxidants such as vitamin E. Lei is currently exploring the paradigm that different types of dietary polyunsaturated fatty acids can selectively modify PCB-induced vascular endothelial cell activation. Omega-6 and omega-3 polyunsaturated fatty acids are the major dietary unsaturated fatty acids, but differ in the position of double bonds, and thus exhibit very unique metabolic properties.
Lei’s studies have shown that supplementation with linoleic acid (the parent omega-6 fatty acid abundant in many vegetable oils) can induce endothelial cell activation, a critical event in the early pathology of atherosclerosis. In contrast, linolenic acid (the parent omega-3 fatty acid abundant in soybean or flax seed oil) can decrease endothelial activation and inflammatory markers. Similar protective properties were observed with omega-3 fatty acids abundant in fish oil. In addition, selected omega-6 fatty acids (e.g., linoleic acid) can potentiate oxidative stress and inflammatory markers induced by coplanar PCBs. Interestingly, by increasing the relative proportions of omega-3 to omega-6 fatty acids, Lei observed downregulation of the PCB-mediated induction of transcription factors critical in the regulation of vascular inflammation.
Lei will continue to explore novel roles of different dietary fatty acids in the regulation of lipid-derived signaling pathways involved in environmental toxicity and inflammatory diseases such as atherosclerosis. There is a great need to further explore this nutritional paradigm in environmental toxicology and to improve our understanding of the relationship between nutrition and lifestyle, exposure to environmental toxins and disease. Nutrition may provide the most sensible means to develop primary intervention and prevention strategies of diseases associated with many environmental toxic insults.
Lei has proven herself as an independent investigator in Dr. Hennig’s laboratory, and completed her dissertation research and received her Ph.D. degree in 2007. Lei is very interested in nutritional modulation of environmental toxins and strongly believes in the goals of the Superfund Basic Research Program and the scientific mission of the Environmental Protection Agency (EPA) and NIEHS. Because of her novel studies in nutrition and environmental toxicology and excellent academic potential, Lei received the University of Kentucky Presidential Fellowship Award for the 2006-2007 academic year, and, following her graduation, worked as a Post Doctorate Research Fellow at Beth Israel Deaconess Medical Center, Harvard University Medical School.