Calcium inhibits promotion by hot dog of 1,2-dimethylhydrazine-induced mucin-depleted foci in rat colon
- PMID: 23712585
- PMCID: PMC3788046
- DOI: 10.1002/ijc.28286
Calcium inhibits promotion by hot dog of 1,2-dimethylhydrazine-induced mucin-depleted foci in rat colon
Abstract
Epidemiology suggests that processed meat is associated with colorectal cancer risk, but few experimental studies support this association. We have shown that a model of cured meat made in a pilot workshop promotes preneoplastic lesions, mucin-depleted foci (MDF) in the colon of rats. This study had two aims: to check if real store-bought processed meats also promote MDF, and to test if calcium carbonate, which suppresses heme-induced promotion, can suppress promotion by processed meat. A 14-day study was done to test the effect of nine purchased cured meats on fecal and urinary biomarkers associated with heme-induced carcinogenesis promotion. Fecal water from rats given hot dog or fermented raw dry sausage was particularly cytotoxic. These two cured meats were thus given to rats pretreated with 1,2-dimethylhydrazine, to evaluate their effect on colorectal carcinogenesis. After a 100-days feeding period, fecal apparent total N-nitroso compounds (ATNC) were assayed and colons were scored for MDF. Hot dog diet increased fecal ATNC and the number of MDF per colon compared with the no-meat control diet (3.0 ± 1.7 vs. 1.2 ± 1.4, p < 0.05). In a third study, addition of calcium carbonate (150 µmol/g) to the hot dog diet decreased the number of MDF/colon and fecal ATNC compared with the hot dog diet without calcium carbonate (1.2 ± 1.1 vs. 2.3 ± 1.4, respectively, p < 0.05). This is the first experimental evidence that a widely consumed processed meat promotes colon carcinogenesis in rats. It also shows that dietary prevention of this detrimental effect is possible.
Keywords: calcium; colorectal cancer; preneoplastic lesions; prevention; processed meat.
Copyright © 2013 UICC.
Conflict of interest statement
This work was supported by French National Institute for Agricultural Research (INRA), the French National Research Agency [PNRA, HemeCancer Project, grant number ANR-05-PNRA-5.E14] and a National Institutes of Health [grant number, RO1-CA-143460].
R.L. Santarelli, as a PhD student, and J.L. Vendeuvre were paid by IFIP (Institut Français du Porc). This article is done “in memoriam” of J.L. Vendeuvre. The other authors disclosed no potential conflicts of interest.
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