Ingestion of viable probiotics or prebiotics is associated with anticarcino
genic effects, one mechanism of which is the detoxification of genotoxins i
n the gut. This mechanism was shown experimentally in animals with use of t
he rat colon carcinogen 1,2-dimethylhydrazine and by determining endpoints
that range from tumorigenesis to induction of DNA damage. Because of the co
mplexity of cancer initiation, cancer progression, and the exposure of canc
er in the gut, many types of interactions may be envisaged. Notably, some o
f our newer studies showed that short-lived metabolite mixtures isolated fr
om milk that was fermented with strains of Lactobacillus bulgaricus and Str
eptococcus thermophilus are more effective in deactivating etiologic risk f
actors of colon carcinogenesis than are cellular components of microorganis
ms. Ingestion of prebiotics results in a different spectrum of fermentation
products, including the production of high concentrations of short-chain f
atty acids. Gut flora, especially after the ingestion of resistant starch,
induces the chemopreventive enzyme glutathione transferase ir in the colon
of the rat. Together, these factors lead to a reduced load of genotoxic age
nts in the gut and to an increased production of agents that deactivate tox
ic components. Butyrate is one such protective agent and is associated with
lowering cancer risk. It was recently shown that buytrate may inhibit the
genotoxic activity of nitrosamides and hydrogen peroxide in human colon cel
ls. In humans, the ingestion of probiotics leads to the excretion of urine
with low concentrations of components that are genotoxic in human colon cel
ls and high concentrations of components that induce oxidized DNA bases.