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Gut metabolites of anthocyanins, gallic acid, 3-O-methylgallic acid, and 2,4,6-trihydroxybenzaldehyde, inhibit cell proliferation of Caco-2 cells.

Abstract
Gut microflora metabolize anthocyanins to phenolic acids and aldehydes. These metabolites may explain the relationship between anthocyanin consumption and reduced incidence of colon cancer. Here, all six major metabolites, along with a Cabernet Sauvignon anthocyanin extract, were incubated with Caco-2 cells at concentrations of 0-1000 microM over 72 h to determine effects on cell proliferation and for 24 h to assess cytotoxicity effects and at 140 microM for 24 h to measure induction of apoptosis. These measurements were based on colorimetric methods. Gallic acid and 3-O-methylgallic acid inhibited cell proliferation and lacked cytotoxicity at low concentrations. The aldehyde metabolite and anthocyanin extract also inhibited cell proliferation at low concentrations and had low cytotoxicity at a wide range of concentrations. Of the four substances that effectively reduced cell proliferation, the aldehyde was the best inducer of apoptosis. In addition, these same four treatments degraded quickly in growth media, suggesting the involvement of subsequent oxidation products in the reduction of cell viability. These results indicate that the anthocyanin microfloral metabolites gallic acid, 3-O-methylgallic acid, and 2,4,6-trihydroxybenzaldehyde reduce cell proliferation in Caco-2 cells more effectively than anthocyanins and may offer protection against colon cancer after their formation in the gut.
AuthorsSarah C Forester, Andrew L Waterhouse
JournalJournal of agricultural and food chemistry (J Agric Food Chem) Vol. 58 Issue 9 Pg. 5320-7 (May 12 2010) ISSN: 1520-5118 [Electronic] United States
PMID20373763 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Anthocyanins
  • Benzaldehydes
  • Gallic Acid
  • 3-O-methylgallic acid
  • 2,4,6-trihydroxybenzaldehyde
Topics
  • Anthocyanins (metabolism, pharmacology)
  • Apoptosis (drug effects)
  • Benzaldehydes (metabolism, pharmacology)
  • Caco-2 Cells
  • Cell Proliferation (drug effects)
  • Gallic Acid (analogs & derivatives, metabolism, pharmacology)
  • Humans

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