Our hypothesis was that administration of bifidobacteria, Lactobacillu
s acidophilus or both to rats will minimize the numbers of aberrant cr
ypts in the distal colon that develop in response to the carcinogen 1,
2-dimethylhydrazine (DMH). A series of experiments was designed to tes
t this hypothesis where the treatments used were as follows: skim milk
controls (Skim-Basal), skim milk + bifidobacteria (Bifido-Basal), ski
m milk + fructooligosaccharide (Skim-FOS), and skim milk + bifidobacte
ria + fructooligosaccharide (Bifido-FOS). In two experiments, bifidoba
cteria + FOS administration significantly decreased the number of aber
rant crypts that developed, but there was no clear relationship of abe
rrant crypts to numbers of bifidobacteria or Clostridium perfringens.
In the third experiment, the Bifido-FOS treatment led to significantly
fewer aberrant crypts and aberrant crypt foci than the Bifido-Basal t
reatment. The Skim-FOS group had significantly more cecal bifidobacter
ia than the Skim-Basal group and significantly fewer C. perfringens th
an the Skim-Basal and Bifido-Basal. In a fourth experiment, L. acidoph
ilus was added as an additional treatment. The number of aberrant cryp
ts was not significantly different among the groups. However, the numb
er of C. perfringens was significantly decreased by the addition of bi
fidobacteria, L. acidophilus or the combination of the two, whereas th
e numbers of bifidobacteria and L. acidophilus were not affected by tr
eatment. A significant correlation (R(2) = 0.84, P < 0.01) was noted b
etween the body weight of rats at DMH administration and the magnitude
of the difference in aberrant crypts between the Skim-Basal rats and
the Bifido-FOS rats. The results suggest that there is variability in
the effects of bifidobacteria and L. acidophilus administration on bot
h aberrant crypt formation and C. perfringens.