Colon concentrations of resveratrol associated with inhibition of AOM‐induced ACF in CF‐1 mice fed piceid‐accumulating transgenic alfalfa with exogenous beta‐glucosidase.

Based on our previous findings, we tested the hypothesis that piceid is not bioavailable from transgenic alfalfa that expresses resveratrol‐synthase. Transgenic alfalfa which contained 193± 18 μg piceid/g dry weight was incorporated into diets at 20% by dry weight and fed to CF‐1 mice for 5 weeks. The supplementation of 860 beta‐glucosidase U/kg diet to transgenic alfalfa and control diets with authentic piceid reduced the number of azoxymethane‐induced ACF in the colon of CF‐1 mice fed these diets by 36% and 41%, respectively, compared to transgenic alfalfa and piceid, alone. Colonic concentrations of resveratrol‐aglycone(< 0.5 nmol/g tissue)in mice fed transgenic alfalfa with enzyme tended to be higher than in animals fed diets without the enzyme supplement (p= 0.09). The use of N‐(n‐butyl)‐deoxygalactonojirimycin (NB‐DGJ), an inhibitor of lactase‐phlorizin hydrolase (LPH), in transport studies with everted jejunal sacs from CF‐1 mice suggested that LPH is involved in the intestinal deglycosylation of piceid. However, the concentration of resveratrol‐aglycone measured in intestinal mucosa preparations incubated in 100 ìM resveratrol‐aglycone was much greater than the amount of piceid and resveratrol‐aglycone detected in the mucosa of intestinal sacs incubated in 100 ìM piceid. Collectively, our studies suggest that the intestinal bioavailability of piceid is much less than that of the aglycone.