Human faeces hydrolysed synthetic β-D-glucuronides of both -nitrophenol and phenolphthalein. The origin of this activity in faeces was localised in the bacterial pellet fraction after centrifugation. Ninety-seven bacterial strains with β-glucuronidase activity isolated from fresh human faeces were identified as species of and They were classified into two groups according to their activity against two synthetic β-D-glucuronides. One group hydrolysed -nitrophenyl glucuronide and phenolphthalein glucuronide to the same extent and the other hydrolysed -nitrophenyl glucuronide much more strongly than phenolphthalein glucuronide. The bile of rats given benzo(a)pyrene by mouth was tested for mutagenicity in the presence and absence of cell-free extracts of human faeces and bacteria. Extracts of β-glucuronidase-positive bacteria increased the mutagenicity of metabolites of benzo(a)pyrene, as did faecal extracts, but extracts of β-glucuronidasenegative bacteria did not. D-Saccharic acid-1, 4-lactone inhibited the increase in mutagenicity produced by the faecal extracts and extracts of β-glucuronidase-positive bacteria except for strains 204 and 952. These results indicate that some intestinal bacteria have β-glucuronidases heterogenous in substrate specificity and that they may be involved in mutagenicity of benzo(a)pyrene in the intestinal tract.


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