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Post-doctoral Research, Rutgers University, Chemical Biology
PhD., The University of Arizona, Pharmacology & Toxicology, 2001
B.S., The Pennsylvania State University, Biochemistry, 1997
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research focus of my laboratory is on the potential obesity and fatty liver disease
preventive effects, as well as, the bioavailability and potential hepatotoxicity
of dietary phytochemicals. Our primary focus currently is on the tea catechin,
(-)-epigallocatechin-3-gallate (EGCG). The
emerging epidemic of obesity, and related complications including fatty liver
disease, makes the development of preventive strategies a key public health concern.
My laboratory is currently studying the effectiveness of EGCG, and other dietary
phytochemicals, as obesity preventive agents with the goal of understanding the
underlying mechanisms of action and maximizing preventive activity using mouse
models. Although
dietary phytochemicals, including EGCG, have a long history of safe use as part
of the diet, there is emerging evidence that high doses of some of these compounds,
given in concentrated dose forms (capsules, tablets, etc.) may cause liver toxicity
in humans. Research in my laboratory is focused on understanding the dose-response
relationships and mechanisms of action underlying these potential toxicities in
mice. We are studying the role of biotransformation and bioavailability in determining
toxic potential of important dietary phytochemicals, and assessing the potential
for phytochemical-drug interactions that could lead to adverse effects.
My laboratory is also interested in the potential lung cancer preventive activities
of dietary phytochemicals either as single agents or in combination with pharmaceutical
compounds. The focus is on establishing efficacy in cell culture and mouse models
of lung cancer and studying the underlying mechanisms of action. |
| | Bose
M, Lambert JD, Ju J, Reuhl KR, Shapses SA, Yang CS. (2008) The major green tea
polyphenol, (-)-epigallocatechin-3-gallate, inhibits obesity, metabolic syndrome,
and fatty liver disease in high-fat fed mice. J Nutr. In press. Lambert
JD, Sang S, Yang CS. (2008) N-Acetylcysteine enhances the lung cancer inhibitory
effect of epigallocatechin-3-gallate and forms a new adduct. Free Rad Biol Med.
44: 1069 - 74. Lambert
JD, Sang S, Yang CS. (2007) Possible controversy over dietary polyphenols: benefits
vs risks. Chem. Res. Toxicol. 20: 583 - 5. Hao
X, Bose M, Lambert JD, Ju J, Lu G, Lee MJ, Park S, Husain A, Wang S, Sun Y, Yang
CS. (2007) Inhibition of tumorigenesis in ApcMin/+ mice by green tea polyphenols
(Polyphenon E) and individual catechins. Nutr. Cancer. 59: 62 - 9. Lambert
JD, Sang S, Yang CS. (2007) Biotransformation of green tea polyphenols and the
biological activities of those metabolites. Mol. Pharmaceutics. 6: 819 - 825.
Bose M, Hao X,
Ju J, Husain A, Park S, Lambert JD, Yang CS. (2007) Inhibition of tumorigenesis
in ApcMin/+ mice by a combination of (-)-epigallocatechin-3-gallate
and fish oil. J. Ag. Food Chem. 55: 7695 - 7700 Lambert
JD, Kwon SJ, Hong, J, Yang CS. (2007) Salivary hydrogen peroxide produced by holding
or chewing green tea in the oral cavity. Free Radical Res. 41: 850 - 53. Lambert
JD, Sang S, Lu AYH, and Yang CS. (2007) Metabolism of dietary polyphenols and
possible interactions with drugs. Current Drug Metabol. 8: 499 - 507. |