The mitochondria as a putative target for the actions of the green tea polyphenol, (-)epigallocatechin-3-gallate

Joshua Lambert, Ph.D., Associate Professor of Food Science, Department of Food Science, The Pennsylvania State University

Date and Location

When (Date/Time)

October 11, 2018, 4:00 PM - 5:00 PM


252 Erickson Food Science Building

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Green tea (Camellia sinensis) is the second most commonly consumed beverage in the world. Both green tea and its major polyphenolic component, (-)-epigallocatechin-3-gallate (EGCG) have been widely studied for the prevention of a number of chronic diseases including cancer, cardiovascular disease, and obesity. Although consumption of green tea beverage is generally regarded as safe, a growing number of studies have indicated that oral bolus treatment with high doses of EGCG can lead to hepatotoxicity in animals; consumption of green tea-based dietary supplements has been associated with case-reports of hepatotoxicity in humans. Data from our laboratory and others have suggested that the ability of EGCG to modulate cellular redox status, either inducing intracellular oxidative stress or antioxidant response, plays a critical role in its bioactivity. The mitochondrion plays a central role in cellular energetics and is the major sources of endogenous reactive oxygen species in the cell. Evolution has positively selected for mechanisms that coordinate mitochondrial biogenesis and the expression of antioxidant response systems. Based on our studies on the selective oral cancer inhibitory effects of EGCG, the mitigation of high fat diet induced fatty liver disease by dietary EGCG, and the induction of hepatotoxicity of oral bolus EGCG, we propose that the mitochondria represents a critical cellular target for EGCG. At dietary doses and in normal cells, EGCG induces a low level of mitochondrial oxidative stress. This leads to enhanced mitochondrial biogenesis and increased expression of cellular antioxidant response systems. At higher doses and/or in cancer cells, EGCG induces higher levels of oxidative stress and inhibition of antioxidant response. In the former case, the effects of EGCG on the mitochondria lead to cytoprotection of normal oral cells or mitigation of fatty liver disease, whereas in the latter case it leads to cancer cell death or hepatotoxicity. Additional studies are needed to more precisely understand the interactions between EGCG and the mitochondrial components, and to demonstrate the most upstream molecular changes that lead to the downstream health-related consequences of EGCG in vivo. Such data should support the design of rationale combination treatments involving EGCG for cancer and obesity, and a greater understanding of potential risk factors for EGCG-related hepatotoxicity