Browsing by Author "Ingman, Tuulia"

Backround and aim of the sudy: Berries and berry polyphenols inhibit the growth of cancerous tumors in vivo and cancer cells in vitro. In the digestive system polyphenols are converted to various metabolites, such as phenolic acids, which may partially count for polyphenol bioactivity. These and other components in the liquid fraction of feces, i.e. the fecal water, are in contact with the proliferating cells residing at the bottom of colonic crypts, and may therefore affect colon cancer risk. The aim of this study was to investigate whether berry consumption changes the effect of fecal water on colon cancer cell viability in vitro, when the amount of dietary red meat is controlled. Also of interest was to investigate the possible correlation between fecal water phenolic acids and the viability of fecal water-exposed cells. Materials and methods: Karnimari was a four-week randomized intervention study with two study groups; one receiving 200 g berries and 150 g pork products daily, and the other group receiving pork products only. Fecal samples were collected before and after intervention and fecal waters were extracted. Polyphenol metabolites from end-point fecal waters were analyzed using UHPLC-DAD-FLD-method. Human colon cancer cells (Caco-2 ja HCA-7) and monkey fibroblasts (CV1-P) were exposed to diluted fecal waters (10 % / 20 % / 30 % fecal water) for 24 h, and cell viability was measured with a method based on cellular dehydrogenase activity. The difference in cell viability between groups after intervention was tested with covariance analysis (ANCOVA). The difference in fecal water concentration of phenolic acids between groups after intervention and the difference in cell viability between groups before intervention were tested with Mann-Whitney U-test. The correlations between fecal water phenolic acids and cell viability were tested with Spearman’s correlation. Results: After intervention fecal waters from the berry group reduced cell viability more than fecal waters from the control group. The difference was significant in all three cell lines when fecal water concentration in cell medium was 30 % (HCA-7 p<0.001; Caco-2 p=0.032; CV1-P p=0.009), and in cells HCA-7 (p=0.007) and CV1-P (p=0.003) also when fecal water concentration was 20 %. The concentrations of fecal water protocathequic acid (p=0.027) and p-coumaric acid (p=0.003) were greater in the berry group than in the control group. p-Coumaric acid concentration was significantly correlated with cell viability in all cell lines when fecal water concentration in cell medium was 20 % or 30 %, regardless of the relatively small amounts of p-coumaric acid detected. Conclusions: Fecal waters from the berry group reduced the viability of both colon cancer cell lines and fibroblasts more than fecal waters from the control group. Eating berries led to greater amounts of protocathequic acid and p-coumaric acid in fecal water. p-Coumaric acid may reduce cell viability or be connected to another affective component in fecal water. The biological mechanisms behind the cell viability reducing ability of fecal water from berry eating subjects should be further investigated.