Endogenous N-nitroso compounds and their precursors present in bacon do not initiate or promote aberrant crypt foci in the colon of rats

摘要

Processed meat intake is associated with increased risk of colorectal cancer. This association may be explained by the endogenous formation of N-nitroso compounds (NOC). The hypothesis that meat intake can increase fecal NOC levels and colon carcinogenesis was tested in 175 F344 rats. Initiation was assessed by the number of aberrant crypt foci (ACF) in the colon of rats, 45 days after the start of a high-fat bacon-based diet. Promotion was assessed by the multiplicity of ACF (crypt/ACF), in rats given experimental diets for 100 d, starting 7 d after an azoxymethane injection. Three promotion studies were done, each in 5 groups of 10 rats, whose diets contained 7, 14 or 28% fat. Tested meats were bacon, pork, chicken and beef. Fecal and dietary NOC were assayed by thermal energy analysis. Results show that feces from rats fed bacon-based diets contained 10 to 20 times more NOC than feces from control rats fed a casein-based diet (all p<0.0001 in four studies). In bacon-fed rats, amount of NOC input (diet) and output (feces) were similar. Rats fed a diet based on beef, pork or chicken meat had less fecal NOC than controls (most p<0.01). No ACF were detected in the colon of bacon-fed uninitiated rats. After azoxymethane injection, unprocessed but cooked meat-based diets did not change the number of ACF, nor the ACF multiplicity, compared with control rats. In contrast, the bacon-based diet consistently reduced the number of large ACF per rat, and the ACF multiplicity in the three promotion studies by 12, 17 and 20 % (all p<0.01). Results suggest that NOC brought by dietary bacon would not enhance colon carcinogenesis in rats.