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EFFECTS OF EGCG ON CYP1A1 PROMOTER ACTIVITY IN MOUSE LIVER CELLS

Abstract

Cancers are prevalent in the world today and difficult to avoid because of their many contributing factors. However, there are some well-known preventative agents present in our diet, including components from green tea extracts. One such chemical is the bioflavonoid, epigallocatechin gallate (EGCG), which inhibits carcinogenic agents, like B[a]P, from binding to the nuclear aryl hydrocarbon receptor (AhR), a transcription factor that binds to DRE sequences in the promoter region of many drug metabolizing genes. One common route of exposure for B[a]P is a diet that includes foods prepared by charcoal grilling. In cells, B[a]P binds to the AhR and activates expression of the Cyp1a1 gene. The protein made from this gene is a drug metabolizing enzyme that also causes the formation of mutagenic metabolites of B[a]P, which can mutate DNA and lead to cancer. In these experiments, we explored the ability of EGCG to inhibit activation of the Cyp1a1 promoter in Hepa 1.1 mouse hepatocytes when treated with an ethanol extract of charcoal-grilled chicken. The results from these studies show a significant decrease in promoter activity when chicken extracts were co-treated with 100 μM EGCG, as determined by a luciferase reporter assay. However, we did not detect any decrease for chicken extracts from well-done (“blackened”) samples. Additionally, we observed 10 μM EGCG treatment decreasing basal levels of Cyp1a1 promoter activity, as compared to the negative control. These data suggest that EGCG may have protective effects against carcinogens that are found in foods common in the diet, like grilled chicken.

Acknowledgements

ACA Ledford Scholarship, YHC Undergraduate Research for the Common Good

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