The Journal of Medical Microbiology, Vol 22, Issue 4 351-355, Copyright © 1986 by Society for General Microbiology
Mutagenic activation of biliary metabolites of benzo(a)pyrene by beta-glucuronidase-positive bacteria in human faeces
M. Nanno, M. Morotomi, H. Takayama, T. Kuroshima, R. Tanaka and M. Mutai
Human faeces hydrolysed synthetic beta-D-glucuronides of both p-nitrophenol
and phenolphthalein. The origin of this activity in faeces was localised in
the bacterial pellet fraction after centrifugation. Ninety-seven bacterial
strains with beta-glucuronidase activity isolated from fresh human faeces
were identified as species of Bacteroides, Peptostreptococcus,
Fusobacterium, Propionibacterium, Clostridium, Eubacterium and
Bifidobacterium. They were classified into two groups according to their
activity against two synthetic beta-D-glucuronides. One group hydrolysed
p-nitrophenyl glucuronide and phenolphthalein glucuronide to the same
extent and the other hydrolysed p-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
beta-glucuronidase-positive bacteria increased the mutagenicity of
metabolites of benzo(a)pyrene, as did faecal extracts, but extracts of
beta-glucuronidase-negative bacteria did not. D-Saccharic acid-1,4-lactone
inhibited the increase in mutagenicity produced by the faecal extracts and
extracts of beta-glucuronidase-positive bacteria except for
Peptostreptococcus strains 204 and 952. These results indicate that some
intestinal bacteria have beta-glucuronidases heterogenous in substrate
specificity and that they may be involved in mutagenicity of benzo(a)pyrene
in the intestinal tract.
