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.

Your Environment. Your Health.

Publication Detail

Title: Epigallocatechin-3-gallate (EGCG) protects against chromate-induced toxicity in vitro.

Authors: Wu, Fen; Sun, Hong; Kluz, Thomas; Clancy, Hailey A; Kiok, Kathrin; Costa, Max

Published In Toxicol Appl Pharmacol, (2012 Jan 15)

Abstract: Hexavalent chromium [Cr(VI)] is a human carcinogen that results in the generation of reactive oxygen species (ROS) and a variety of DNA lesions leading to cell death. Epigallocatechin-3-gallate (EGCG), the major polyphenol present in green tea, possesses potent antioxidative activity capable of protecting normal cells from various stimuli-induced oxidative stress and cell death. Here we demonstrated that co-treatment with EGCG protected human normal bronchial epithelial BEAS-2B cells from Cr(VI)-induced cell death in a dose-dependent manner. Cr(VI) induces apoptosis as the primary mode of cell death. Co-treatment of BEAS-2B cells with EGCG dose-dependently suppressed Cr(VI)-induced apoptosis. Fluorescence microscopic analyses and quantitative measurement revealed that EGCG significantly decreased intracellular levels of ROS induced by Cr(VI) exposure. Using a well-established K(+)/SDS precipitation assay, we further showed that EGCG was able to dose-dependently reduce DNA-protein cross-links (DPC), lesions that could be partially attributed to Cr(VI)-induced oxidative stress. Finally, analyses of Affymetrix microarray containing 28,869 well-annotated genes revealed that, among the 3412 genes changed more than 1.5-fold by Cr(VI) treatment, changes of 2404 genes (70%) were inhibited by pretreatment of EGCG. Real-time PCR confirmed the induction of 3 genes involved in cell death and apoptosis by Cr(VI), which was eliminated by EGCG. In contrast, Cr(VI) reduced the expression of 3 genes related to cellular defense, and this reduction was inhibited by EGCG. Our results indicate that EGCG protects BEAS-2B cells from Cr(VI)-induced cytotoxicity presumably by scavenging ROS and modulating a subset of genes. EGCG, therefore, might serve as a potential chemopreventive agent against Cr(VI) carcinogenesis.

PubMed ID: 22079256 Exiting the NIEHS site

MeSH Terms: Antioxidants/administration & dosage; Antioxidants/pharmacology*; Apoptosis/drug effects; Bronchi/cytology; Bronchi/drug effects; Bronchi/pathology; Carcinogens, Environmental/toxicity*; Catechin/administration & dosage; Catechin/analogs & derivatives*; Catechin/pharmacology; Chromium/toxicity*; Dose-Response Relationship, Drug; Epithelial Cells/drug effects; Epithelial Cells/pathology; Free Radical Scavengers/administration & dosage; Free Radical Scavengers/pharmacology; Gene Expression Regulation/drug effects; Humans; Microscopy, Fluorescence; Oligonucleotide Array Sequence Analysis; Polymerase Chain Reaction; Reactive Oxygen Species/metabolism*

Back
to Top