Ingestion of viable probiotics or
prebiotics is associated with
anticarcinogenic effects, one mechanism of which is the detoxification of
genotoxins in the gut. This mechanism was shown experimentally in animals with use of the rat colon
carcinogen 1,2-dimethylhydrazine and by determining endpoints that range from
tumorigenesis to induction of DNA damage. Because of the complexity of
cancer initiation,
cancer progression, and the exposure of
cancer in the gut, many types of interactions may be envisaged. Notably, some of our newer studies showed that short-lived metabolite mixtures isolated from milk that was fermented with strains of Lactobacillus bulgaricus and Streptococcus thermophilus are more effective in deactivating etiologic risk factors of colon
carcinogenesis than are cellular components of microorganisms. Ingestion of
prebiotics results in a different spectrum of fermentation products, including the production of high concentrations of
short-chain fatty acids. Gut flora, especially after the ingestion of
resistant starch, induces the chemopreventive
enzyme glutathione transferase pi in the colon of the rat. Together, these factors lead to a reduced load of genotoxic agents in the gut and to an increased production of agents that deactivate toxic 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 cells. In humans, the ingestion of probiotics leads to the excretion of urine with low concentrations of components that are genotoxic in human colon cells and high concentrations of components that induce oxidized
DNA bases.