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Stratégies préventives de la cancérogénèse colorectale

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Fiche n° 19 : maîtrise des qualités nutritionnelles des produits

L'IFIP a participé au programme Sécuriviande coordonné par Toxalim (INRA Toulouse) dans l’optique d’identifier les solutions technologiques permettant de réduire les lésions précancéreuses des produits carnés sur le modèle rat.
Alors que l’IARC (Centre International de Recherche sur le Cancer) vient de classer les charcuteries dans le groupe 1 des produits cancérigènes, ce projet vise à démontrer que certaines solutions technologiques simples existent pour éliminer tout lien entre charcuterie et cancer.
Ce travail de haut niveau scientifique a permis d’identifier les mécanismes d’action du fer via l’oxydation et la production de NOCs (composés N-nitrosés potentiellement cancérigènes) dans les fèces. Ce projet étudie aussi comment ces NOCs interviennent dans l’altération de la muqueuse colique sur les rats chimio induits.
Complémentaire au programme Hèmecancer, Sécuriviande a permis de démontrer que le calcium d’une part, et certains antioxydants d’autre part, sont efficaces pour éliminer la production de NOCs chez l’homme et l’apparition de lésions coliques chez le rat chimio induit.
Ce programme a enfin testé l’acceptation sensorielle de solutions antioxydantes proposées auprès de groupes de consommateurs « naïfs ».

PDF icon fiche_bilan2015_019.pdf
2016

Calcium inhibits promotion by hot dog of 1,2-dimethylhydrazine-induced mucin-depleted foci in rat colon

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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.

2013

Calcium and a-tocopherol suppress cured-meat promotion of chemically induced colon carcinogenesis in rats and reduce associated biomarkers in human volunteers1–3

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Background: Processed meat intake has been associated with increased colorectal cancer risk. We have shown that cured meat promotes carcinogen-induced preneoplastic lesions and increases specific biomarkers in the colon of rats.
Objectives: We investigated whether cured meat modulates biomarkers of cancer risk in human volunteers and whether specific agents can suppress cured meat–induced preneoplastic lesions in rats and associated biomarkers in rats and humans.
Design: Six additives (calcium carbonate, inulin, rutin, carnosol, a-tocopherol, and trisodium pyrophosphate) were added to cured meat given to groups of rats for 14 d, and fecal biomarkers were measured. On the basis of these results, calcium and tocopherol were kept for the following additional experiments: cured meat, with or without calcium or tocopherol, was given to dimethylhydrazine-initiated rats (47% meat diet for 100 d) and to human volunteers in a crossover study (180 g/d for 4 d). Rat colons were scored for mucin-depleted foci, putative precancer lesions. Biomarkers of nitrosation, lipoperoxidation, and cytotoxicity were measured
in the urine and feces of rats and volunteers.
Results: Cured meat increased nitroso compounds and lipoperoxidation in human stools (both P , 0.05). Calcium normalized both biomarkers in rats and human feces, whereas tocopherol only decreased nitro compounds in rats and lipoperoxidation in feces of volunteers (all P , 0.05). Last, calcium and tocopherol reduced the number of mucin-depleted foci per colon in rats compared with nonsupplemented cured meat (P = 0.01).
Conclusion: Data suggest that the addition of calcium carbonate to the diet or a-tocopherol to cured meat may reduce colorectal cancer risk associated with cured-meat intake. This trial was registered at clinicaltrials. gov as NCT00994526.

2013

Meat processing and colon carcinogenesis : cooked, nitrite-treated and oxidized high-heme cured meat promotes mucin depleted foci in rats

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Processed meat intake is associated with colorectal cancer risk, but no experimental study supports the epidemiologic evidence. To study the effect of meat processing on carcinogenesis promotion, we first did a 14-day study with 16 models of cured meat. Studied factors, in a 2 × 2 × 2 × 2 design, were muscle color (a proxy for heme level), processing temperature, added nitrite, and packaging. Fischer 344 rats were fed these 16 diets, and we evaluated fecal and urinary fat oxidation and cytotoxicity, three biomarkers of heme-induced carcinogenesis promotion.
2010