Skip Navigation
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

National Institute of Environmental Health Sciences

Use this QR code to view the newest version of this document
Use this QR code to view the newest version of this document

Your Environment. Your Health.

Publication Detail

Title: Pro-oxidative activities and dose-response relationship of (-)-epigallocatechin-3-gallate in the inhibition of lung cancer cell growth: a comparative study in vivo and in vitro.

Authors: Li, Guang-Xun; Chen, Yu-Kuo; Hou, Zhe; Xiao, Hang; Jin, Huanyu; Lu, Gary; Lee, Mao-Jung; Liu, Ba; Guan, Fei; Yang, Zhihong; Yu, Albert; Yang, Chung S

Published In Carcinogenesis, (2010 May)

Abstract: (-)-Epigallocatechin-3-gallate (EGCG), the major polyphenol in green tea, has been shown to inhibit tumorigenesis and cancer cell growth in animal models. Nevertheless, the dose-response relationship of the inhibitory activity in vivo has not been systematically characterized. The present studies were conducted to address these issues, as well as the involvement of reactive oxygen species (ROS), in the inhibitory action of EGCG in vivo and in vitro. We characterized the inhibitory actions of EGCG against human lung cancer H1299 cells in culture and in xenograft tumors. The growth of tumors was dose dependently inhibited by EGCG at doses of 0.1, 0.3 and 0.5% in the diet. Tumor cell apoptosis and oxidative DNA damage, assessed by the formation of 8-hydroxy-2'-deoxyguanosine (8-OHdG) and phosphorylated histone 2A variant X (gamma-H2AX), were dose dependently increased by EGCG treatment. However, the levels of 8-OHdG and gamma-H2AX were not changed by the EGCG treatment in host organs. In culture, the growth of viable H1299 cells was dose dependently reduced by EGCG; the estimated concentration that causes 50% inhibition (IC(50)) (20 microM) was much higher than the IC(50) (0.15 microM) observed in vivo. The action of EGCG was mostly abolished by the presence of superoxide dismutase (SOD) and catalase, which decompose the ROS formed in the culture medium. Treatment with EGCG also caused the generation of intracellular ROS and mitochondrial ROS. Although EGCG is generally considered to be an antioxidant, the present study demonstrates the pro-oxidative activities of EGCG in vivo and in vitro in the described experimental system.

PubMed ID: 20159951 Exiting the NIEHS site

MeSH Terms: Animals; Anticarcinogenic Agents/pharmacology*; Apoptosis/drug effects; Catechin/analogs & derivatives*; Catechin/pharmacokinetics; Catechin/pharmacology; Cell Line, Tumor; Cell Proliferation/drug effects; DNA Damage; DNA Repair/drug effects; Deoxyguanosine/analogs & derivatives; Deoxyguanosine/biosynthesis; Dose-Response Relationship, Drug; Histones/biosynthesis; Humans; Lung Neoplasms/drug therapy*; Lung Neoplasms/pathology; Male; Membrane Potential, Mitochondrial/drug effects; Mice; Oxidative Stress; Reactive Oxygen Species/metabolism; Xenograft Model Antitumor Assays

Back
to Top