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

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.

Luteolin inhibits Cr(VI)-induced malignant cell transformation of human lung epithelial cells by targeting ROS mediated multiple cell signaling pathways

“…Inhibition of metal induced carcinogenesis by a dietary antioxidant is a novel approach. Studies have demonstrated that co-treatment with Epigallocatechin-3-gallate (EGCG), the major polyphenol present in green tea, protected BEAS-2B cells from Cr(VI)-induced cell death in a dose-dependent manner (Wu et al , 2012). …”

Epigallocatechin gallate protects BEAS-2B cells from lipopolysaccharide-induced apoptosis through upregulation of gastrin-releasing peptide

“…Protective effect of EGCG against SNP-induced apoptosis in L-132 human lung epithelial cells was exerted by regulating the expression of Bax and Bcl-2 as well as the activity of caspase-3 [16]. EGCG protected the BEAS-2B cells from chromate-induced toxicity by reducing ROS levels as well as by inhibiting the expression of apoptosis-related genes [18]. The protective properties of EGCG on toxic chemical-induced apoptosis are associated with its ability to upregulate transcription factors such as Nrf2 [19] or prevent the degradation of positive growth effectors such as HIF-1 [20].…”

Rutin inhibits proliferation, attenuates superoxide production and decreases adhesion and migration of human cancerous cells

“…Nevertheless, it was previously described the dietary intervention of polyphenols in cancer prevention, including the chemopreventive ability of dietary flavonoids, act against lung carcinogens. In vitro studies were performed over a wide range of polyphenols which showed significant effect in lung Cancer, such as epigallocatechin-3-gallate (EGCG), suppresses in a dose dependent manner, the hexavalent chromium (Cr (VI))-induced apoptosis, reduces activation of caspase-3 and nuclear poly (ADP-ribose) polymerase (PARP), and intracellular ROS [9]. It has also been demonstrated, that Caffeic acid can scavenge intracellular ROS and hence prevent lipid peroxidation in WI-38 cells [10].…”