Beer is a relatively rich source of phytochemicals, including phenolic acids, hydroxycinnamates and flavonoids(Reference Pascoe, Ames and Chandra1). Such compounds, also present in a variety of foods, are widely reported for their protective effect in chronic disease development(Reference Knekt, Kumpulainen and Jarvinen2). The physiological function of polyphenols in vivo is dependent on the extent of their absorption and metabolism in the gastrointestinal tract. Flavonols are metabolised to O-methylated, glucuronide and sulphate conjugates during absorption in the small intestine(Reference Spencer, Chowrimootoo and Choudhury3). The majority of these metabolites are not transferred across the jejunum or ileum and as a result reach the large intestine intact, where they may impart biological activity(Reference Corona, Deiana and Incani4).
The polyphenol contents of lager, ale and stout and their link to antioxidant potential were investigated. Ethyl acetate and aqueous extracts were prepared from each beer. Ale extracts were found to contain the highest level of polyphenols (3196 mg gallic acid equivalents/l) and to possess the highest antioxidant activity (3525 μm Trolox equivalent). To better characterise the polyphenol content of ale, centrifugal partition chromatography (CPC) was used to separate ale extracts into seventeen fractions, which were further analysed by reverse-phase HPLC and liquid chromatography–(electrospray ionization)–MS–MS. Measurable polyphenol content and total phenolic content within CPC fractions was shown to be positively correlated with antioxidant activity (R 2 0.741, P<0.05). In addition, quercetin derivatives and myricetin were identified, which correlate well with antioxidant potential.
The absorption of beer prenylated flavonoids across Caco-2 cell monolayers was investigated and pH-controlled stirred batch-culture vessels were used as an in vitro model of colonic metabolism.
The anti-proliferative effect of beer phytochemicals and beer extracts on human colon adenocarcinoma cells was also investigated. Caco-2 cells seeded in twelve-well plates (1.2×104 cells/ml) were grown for 4 d before exposure to lager, ale or stout extracts (50 μg/ml), flavonol solutions (1–100 μm) or vehicle (1% (v/v) methanol or 1% (v/v) dimethyl sulfoxide) for 24, 48, 72 and 96 h before sulforhodamine B assays (Sigma-Aldrich, Poole, Dorset, UK) were performed to evaluate total biomass. Stout produced a moderate inhibitory effect on cancer cell proliferation, whilst myricetin exerted a strong inhibitory effect.
Figure. (A) Growth inhibition by beer extracts (n 9); (B) growth inhibition by myricetin (n 2). Values are means and 1 sd represented by vertical bars.
V. J. C. is in receipt of a BBSRC CASE Studentship with BRI.
