Effect of processed and red meat on endogenous nitrosation and DNA damage

Joosen, A. M.C.P., Kuhnle, G. G.C. ORCID: https://orcid.org/0000-0002-8081-8931, Aspinall, S. M., Barrow, T. M., Lecommandeur, E., Azqueta, A., Collins, A. R. and Bingham, S. A. (2009) Effect of processed and red meat on endogenous nitrosation and DNA damage. Carcinogenesis, 30 (8). pp. 1402-1407. ISSN 0143-3334 doi: 10.1093/carcin/bgp130

Abstract/Summary

Haem in red meat (RM) stimulates the endogenous production of mutagenic nitroso compounds (NOC). Processed (nitrite-preserved red) meat additionally contains high concentrations of preformed NOC. In two studies, of a fresh RM versus a vegetarian (VEG) diet (six males and six females) and of a nitrite-preserved red meat (PM) versus a VEG diet (5 males and 11 females), we investigated whether processing of meat might increase colorectal cancer risk by stimulating nitrosation and DNA damage. Meat diets contained 420 g (males) or 366 g (females) meat/per day. Faecal homogenates from day 10 onwards were analysed for haem and NOC and asso- ciated supernatants for genotoxicity. Means are adjusted for differ- ences in male to female ratios between studies. Faecal NOC concentrations on VEG diets were low (2.6 and 3.5 mmol/g) but significantly higher on meat diets (PM 175 ± 19 nmol/g versus RM 185 ± 22 nmol/g; P 5 0.75). The RM diet resulted in a larger pro- portion of nitrosyl iron (RM 78% versus PM 54%; P < 0.0001) and less nitrosothiols (RM 12% versus PM 19%; P < 0.01) and other NOC (RM 10% versus PM 27%; P < 0.0001). There was no statis- tically significant difference in DNA breaks induced by faecal water (FW) following PM and RM diets (P 5 0.80). However, PM re- sulted in higher levels of oxidized pyrimidines (P < 0.05). Surpris- ingly, VEG diets resulted in significantly more FW-induced DNA strand breaks than the meat diets (P < 0.05), which needs to be clarified in further studies. Meats cured with nitrite have the same effect as fresh RM on endogenous nitrosation but show increased FW-induced oxidative DNA damage.

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Item Type	Article
URI	https://reading-clone.eprints-hosting.org/id/eprint/28633
Identification Number/DOI	10.1093/carcin/bgp130
Refereed	Yes
Divisions	Life Sciences > School of Chemistry, Food and Pharmacy > Department of Food and Nutritional Sciences > Human Nutrition Research Group
Additional Information	The full text of this article is freely available via PMC using the link supplied in Related URLs
Publisher	Oxford University Press
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