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ETHANOL EXTRACTS MADE FROM CHICKEN GRILLED WITH CHARCOAL, BUT NOT PROPANE, SHOW HIGH AHR ACTIVATION IN MOUSE LIVER CELLS

Abstract

Benzo[a]pyrene (B[a]P), a polycyclic aromatic hydrocarbon and agonist of the aryl hydrocarbon receptor (AhR), is produced when meat is burnt. Over consumption of burnt meat can cause increased levels of B[a]P, thus increasing AhR activation and the likelihood of developing cancer. Certain bioflavonoids have been shown to inhibit AhR activation, thus preventing overexpression of down-stream gene products, like CYP1A1. Research suggests that B[a]P is still present even in meat not considered completely burnt. This prompted the examination of different cooking methods on levels of AhR activation in cooked chicken samples. We further addressed the ability of epicatechin, a bioflavonoid found in dark chocolate, to reduce AhR activation. Mouse liver cells were exposed to ethanol extracts of charcoal-grilled or propane-grilled chicken. Epicatechin was tested over a range of concentrations (25, 50, 100, and 200µM). A CYP1A1-promoter luciferase reporter assay was used to determine AhR activity. Data indicate a significant difference in AhR activation between the charcoal grilled and propane grilled chicken (P<0.001), with samples prepared with charcoal exhibiting 10.1-fold higher levels than those prepared with propane. None of the concentrations of epicatechin examined showed a significant reduction of AhR activation in the presence of charcoal-grilled chicken, however the 200 µM concentration of epicatechin alone activated the AhR 4.4-fold over the control (P<0.001). Together, these results suggest that propane-grilled chicken may be a safer alternative to charcoal-grilled chicken. We are unable to provide evidence that epicatchin inhibits the AhR to act as a method of chemoprevention.

Acknowledgements

Young Harris College Undergraduate Research for the Common Good Fund

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