The potential of intestinal bacteria to hydrolyze ginsenoside Rb1 to 20-O-beta-D-glucopyranosyl-20(S)-protopanaxadiol (I) was found in 79% of the fecal specimens from 58 human subjects whose age ranged from 1 to 64 years. Following a ginsenoside-Rb1-hydrolyzing activity assay, Prevotella oris strains were then isolated as a major bacterial species possessing the potential. All the intestinal isolates converted ginsenosides Rb1 and Rd to I, ginsenoside Rb2 to 20-O-[alpha-L-arabinopyranosyl(1-->6)-beta-D-glucopyranosyl]-20(S) -protopanaxadiol (II), and ginsenoside Rc to 20-O-[alpha-L-arabinofuranosyl(1-->6)-beta-D-glucopyranosyl]-20(S)- protopanaxadiol (III) like fecal microflora, but did not attack ginsenosides Re or Rg1 (protopanaxatriol-type). The isolates were susceptible to colimycin (MIC, 3.13 micrograms/ml) and then the treatment of specific pathogen free mice with colimycin (20 mg/kg/day) decreased intestinal bacterial Rb1-hydrolyzing potential from 22.1 +/- 1.2% to 4.7 +/- 2.7%, while the decreased potential was restored to 30.7 +/- 3.7% by the inoculation with P. oris isolates. These results suggest that the metabolism of protopanaxadiol saponins to metabolites I-III in the intestines seems most partly due to intestinal P.oris. In addition, the fact that neither intact ginsenoside Rb1 nor its middle metabolic derivatives but only the final metabolite I was detected at 1.0-7.3 micrograms/ml in blood after oral administration of mice with ginsenoside Rb1 (125 mg/kg) allows us to speculate that metabolites I-III are the most likely forms of protopanaxadiol saponins absorbed from the intestines.