M. Wilpart

Anti-initiation activity of N-acetylcysteine in experimental colonic carcinogenesis

N-Acetylcysteine (NAC) is a soluble nucleophile that has been shown to have antimutagenic activity towards various genotoxic agents including 1,2-dimethylhydrazine (DMH). The present report extends such observations by showing the protective effect of NAC against the carcinogenic activity of DMH. This thiol-containing molecule reduced the incidence of rat intestinal tumors. Moreover, it significantly lowered the colic tumor yield as expressed by the number of tumors per rat bearing tumors. With regard to localisation of colic carcinomas, NAC induced a shift from distal to more proximal sites.

Intestinal carcinogenesis and dietary fibers: the influence of cellulose or Fybogel chronically given after exposure to DMH.

This study was initiated to analyze the effect of a) two characterized vegetal fibers [i.e., a polysaccharide (cellulose) and a mucilaginous substance (Fybogel)], which were b) added at two concentrations (5% and 15% wt/wt), c) as constituents of low (5% wt/wt) and high (20% wt/wt) fat isocaloric diets d) given chronically to rats one week after the administration of 1,2-dimethylhydrazine (DMH); DMH had previously been injected once a week for 15 weeks to induce intestinal carcinogenesis. The dietary consumption, the body weight, and the fecal outflow showed a similar and regular evolution for the rats of all experimental groups; the exception was those receiving the 20% lipids-15% Fybogel diet. That specific diet caused a decrease in body weight concomitant with an increase in dietary consumption and in fecal outflow. The variation in fecal outflow depended on fat and fiber concentrations. The mucilage was more degraded, in absolute and relative amount, than was cellulose when this polysaccharide was included at a 20% lipid diet. Concerning the effect of these two fibers on intestinal carcinogenesis, Fybogel showed an anticarcinogenic property, whereas cellulose did not. The inhibitory activity of Fybogel was on the incidence of intestinal and colonic tumors as well as on the colonic tumor yield. Moreover, it slowed down the rate of colonic formation.

Lipids and Colonic Carcinogenesis: Fact or Artefact?

Life style and dietary habits play an important role in the causation and development of a number of major human cancers1. This conclusion is partly supported by evidence from epidemiological and laboratory animal studies. Investigators have attempted to study the mechanisms by which diet may influence carcinogenesis and to examine the ability of nutrients, food components or non-nutritive food additive components to enhance or to inhibit carcinogenesis. Cancer of the colon is one of the most common tumors observed in the affluent western populations2 for which the relationship between epidemiological and laboratory findings and an overall assessment of the influence of diet on carcinogenesis is not straight forward.