Aims: Conjugated hydroxycinnamates, such as chlorogenic acid (caffeoyl-quinic acid), are widely consumed in a Western diet, coffee being one of the richest sources. Ingested hydroxycinnamate esters can reach the large intestine essentially unaltered, and may then be hydrolysed by esterases produced by the indigenous micro¯ora. This study is aimed at identifying bacterial species responsible for the release of natural antioxidants, such as hydroxycinnamic acids, in the human large intestine. Methods and Results: Thirty-®ve isolates recovered after anaerobic batch culture incubation of human faecal bacteria in a chlorogenic acid-based medium were screened for cinnamoyl esterase activity. Six isolates released the hydroxycinnamate, ferulic acid, from its ethyl ester in a plate-screening assay, and these were identi®ed through genotypic characterization (16S rRNA sequencing) as Escherichia coli (three isolates), Bi®dobacterium lactis and Lactobacillus gasseri (two strains). Chlorogenic acid hydrolysing activities were essentially intracellular. These cinnamoyl esterase-producing organisms were devoid of other phenolic-degrading activities. Conclusions:The results show that certain gut bacteria, including some already recognized as potentially health-promoting (i.e. species belonging to the genera Bi®dobacterium and Lactobacillus), are involved in the release of bioactive hydroxycinnamic acids in the human colon. Signi®cance and Impact of the Study: Free hydroxycinnamates, including caffeic, ferulic and p-coumaric acids, exhibit antioxidant and anticarcinogenic properties both in vitro and in animal models. Given that the gut¯ora has a major role in human nutrition and health, some of the bene®cial effects of phenolic acids may be ascribed to the micro¯ora involved in metabolism.

Flavonoids and cinnamates are widespread phenolic secondary metabolites synthesized by plants for defensive purposes. Many foods and beverages contain high levels of phenolic compounds. Certain phenolics in the diet are particularly bioactive and have pronounced effects on mammalian cells. These effects, together with epidemiological studies and animal models, have led to the hypothesis that dietary phenolics contribute to the health benefits of a diet rich in fruit and vegetables. This paper examines the biochemistry of the uptake and metabolic route of two groups of plant phenolics, the flavonols and hydroxycinnamates.

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The ester-linked ferulic acid of wheat bran and sugar-beet pulp can be con¨erted to¨anillin using biological transformation. Free ferulic acid from sugar-beet pulp and from wheat bran was almost quantitati¨ely obtained by extensi¨e degradation of the cell-walls using enzyme mixtures complemented with specific ferulic acid esterases. The Basidiomycete Pycnoporus cinnabarinus then con¨erted the released ferulic acid to¨anillin. The selection of stable and highly producti¨e strains was achie¨ed using formal ( ) genetics. The use of cellobiose as an acti¨ator of the¨anillin pathway, and the sequential addition of a precursor ferulic acid in cultures of selected P. cinnabarinus strains, allowed 90 and 300 mg r L of¨anillin to be obtained from ferulic acid enzymically released from wheat bran and sugar-beet pulp, respecti¨ely. This process was adapted into a two-step process in¨ol¨ing two filamentous fungi, Aspergillus niger and P. cinnabarinus, with complementary capabilities of transformation.

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Ferulic acid, derived from sugar beet pulp, was used as precursor in a biotechnological two‐step process to produce‘natural’ vanillin. This process combined the biotransformation of sugar beet pulp ferulic acid to vanillic acid by a micromycete, Aspergillus niger and the biotransformation of recovered vanillic acid into vanillin by a basidiomycete, Pycnoporus cinnabarinus. The system produced more than 100 mg litre−1 natural vanillin. The sensorial analysis of this new natural vanillin revealed, besides a predominant vanillin flavour, a slight odour of chocolate as a secondary organoleptic sensation. © 1999 Society of Chemical Industry

A disease such as cancer, where a number of alterations to normal cell function accumulate over time, presents several chernopreventive opportunities to inhibit, slow down or even reverse the process. Many of the crucial changes are induced by alterations to cell signalling pathways which regulate proliferation and apoptosis. As our knowledge of these complicated signalling networks improves, it is becoming clear that many molecules, both drugs and naturally occumng dietary constituents can interact beneficially with deregulated pathways. Molecules such as aspirin and other non-steroidal antiinflammatory drugs, as well as many dietary plant components, for example from green vegetables and tea, can inhibit signalling by affecting kinase activity and therefore phosphorylation of key molecules. Examples of pathways which can be modulated by these agents include activation of the transcription factor nuclear factor-* by tumour promoton or cytokines, signalling by growth factors through the epidermal growth factor receptor/mitogen activated protein kinase pathway and the stress activated (SAF'K)/p38 pathways. Evidence exists, at least from in virro experiments, that through targetting signalling pathways, some compounds may be able to restore rates of apoptosis and proliferation to normal levels, thus rendering them relatively non-toxic, an essential requirement for a good chemopreventive agent.c12 Diet and colorectal cancer prevention MRC Dunn Human Nutrition Unit. Hills Road, Cambridge CB2 2DH Colorectal cancer is the second most common cancer in the UK. The majority of cancers are sporadic and epidemiological estimates suggest that up to 80% of colorectal cancer is attributable to diet This means that it is potentially a preventable disease. Epidemiologically, cross sectional comparisons, case control studies and trends in food intakes show high rates of colorectal cancer in populations consuming diets high in meat and far, and low in starch, NSP (non starch polysaccharides. fibre) and vegetables. In general, prospective studies tend to support these findings although estimates of relative risk are not high. Existing prospective studies have however used crude indices of diet subject to substantial measurement error, and interactions with genetic polymorphisms in for example phase I and I1 enzymes have been studied only rarely. The association between meat consumption and colorectal cancer is usually attributed to the formation of heterocyclic amines in meat when it is cooked. In addition, in humans high meat diets increase the level of nitrosatable material entering the colon so that faecal N-nitrosocompounds (NOC) increase in a dose rcponsivc manner following endogenous synthesis in the colon. Some of the mutations and guanine adducts accumulated during colorcctal cancer progression are characteristic of alkylative damage which would be compatible with N O C exposure. To date, NSP, resistant starch and vegetables have not reduced faecal N O C levels. C13 Human metabolism of dietary chemopreventive compounds Gary...