Probiotics reduce the risk of colon cancer by inhibiting carcinogen-induced DNA damage in animals, but there are no analogous data in human subjects. To enhance knowledge of the effects of probiotics in human subjects, we have investigated the genotoxicity of faecal water after dietary intervention with standard yoghurt or with probiotic yoghurt, which included the strains Lactobacillus acidophilus 145 and Bifidobacterium longum 913. Faeces were collected from nine healthy volunteers after intervention with probiotic yoghurt or standard yoghurt. Faecal water was isolated and incubated with human colon tumour cells HT29clone19A. DNA strand breaks, oxidised DNA bases and damage after challenge with H2O2 were determined by micro-gel-electrophoresis. Faecal water was genotoxic in comparison with NaCl, but protected against H2O2-induced DNA strand breaks. The intervention with probiotic yoghurt significantly lowered faecal water genotoxicity compared with standard yoghurt. However, probiotic intervention also increased oxidative damage; this either reflected prooxidative activity or stimulation of endogenous defence systems. Altogether, the balance of effects favoured protection, since faecal water from the probiotic group reduced overall genetic damage. Thus, there was a reduction of strand break-inducing compounds in human faeces after dietary intervention with probiotic bacteria. This protection reflected results from previous studies in carcinogen-exposed animals where probiotics reduced DNA damage in colon cells.

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Dietary intervention with the probiotics Lactobacillus acidophilus 145 and Bifidobacterium longum 913 modulates the potential of human faecal water to induce damage in HT29clone19A cells

Determination of pyrrolizidine alkaloids in commercial comfrey products (Symphytum sp.)

In the last 15 years the hypothetical concept of cocarcinogenesis has been substantiated by chemical, biochemical, and biologic investigation of the polyfunctional, diterpene mono- and diester type promoters (and stimulators) of initiation, originating from plant species. Thus, the long suspected concept of amplification of carcinogenesis by non-carcinogens was finally established. In addition, the new principle of “cryptic” cocarcinogens was detected in the form of low activity 20-esters of corresponding highly active polyfunctional diterpene mono- and diesters. Cryptic cocarcinogens require metabolic activation by esterases or lipases to become directly acting promoters and/or stimulators of initiation.

Cocarcinogenesis and tumor promoters of the diterpene ester type as possible carcinogenic risk factors.

Smoking is made responsible for a variety of cancers in man and it is estimated that some 30% of all cancer deaths in the USA are caused by smoking (Doll and Peto 1981; The Health Consequences of Smoking 1982; Smoking and Health 1979). The finding that cigarette smoke is mutagenic in a variety of test systems including somatic cells of man may be helpful to a better understanding of the mechanisms by which smoking leads to cancer. These data also support the mutation theory of the origin of cancer which was already formulated by Boveri in 1914 and elaborated by Bauer in 1928 (see also Bauer 1963).

Mutagenic Activity of Cigarette Smoke

The Paradigm of Two-Stage Carcinogenesis: A Critical Attitude

http://academic.oup.com/milmed/article-pdf/146/3/176/24126202/milmed-146-3-176a.pdf

Elliot Perlin

Papers

Naturally Occuring Carcinogens, Mutagens, and Modulators of Carcinogenesis