Biology:Nitrosamine formation during digestion

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In biochemistry, nitrosamines are a class of compounds that can form during food digestion. The presence of their precursors, nitrites, in cured meats, is controversial, because of a small connection to cancer risk.

Background

Nitroso compounds react with primary amines in acidic environments to form nitrosamines, which human metabolism converts to mutagenic diazo compounds. Small amounts of nitro and nitroso compounds form during meat curing; the toxicity of these compounds preserves the meat against bacterial infection. After curing completes, the concentration of these compounds appears to degrade over time. Their presence in finished products has been tightly regulated since several food-poisoning cases in the early 20th century,[1] but consumption of large quantities of processed meats can still cause a slight elevation in gastric and oesophageal cancer risk today.[2][3][4][5]

For example, during the 1970s, certain Norway farm animals began exhibiting elevated levels of liver cancer. These animals had been fed herring meal preserved with sodium nitrite. The sodium nitrite had reacted with dimethylamine in the fish and produced dimethylnitrosamine.[6]

The effects of nitroso compounds vary dramatically across the gastrointestinal tract, and with diet. Nitroso compounds present in stool do not induce nitrosamine formation, because stool has neutral pH.[7][8] Stomach acid does cause nitrosamine compound formation, but the process is inhibited when amine concentration is low (e.g. a low-protein diet or no fermented food). The process may also be inhibited in the case of high vitamin C (ascorbic acid) concentration (e.g. high-fruit diet).[9][10][11] However, when 10% of the meal is fat, the effect reverses, and ascorbic acid markedly increases nitrosamine formation.[12][13]

References

  1. ↑ Honikel, K. O. (2008). "The use an control of nitrate and nitrite for the processing of meat products". Meat Science 78 (1–2): 68–76. doi:10.1016/j.meatsci.2007.05.030. PMID 22062097. http://innocua.net/web/download-2035/1-s2.0-s0309174007001994-main.pdf. 
  2. ↑ Lunn, J.C.; Kuhnle, G.; Mai, V.; Frankenfeld, C.; Shuker, D.E.G.; Glen, R. C.; Goodman, J.M.; Pollock, J.R.A. et al. (2006). "The effect of haem in red and processed meat on the endogenous formation of N-nitroso compounds in the upper gastrointestinal tract". Carcinogenesis 28 (3): 685–690. doi:10.1093/carcin/bgl192. PMID 17052997. https://academic.oup.com/carcin/article/28/3/685/2476497. 
  3. ↑ Bastide, Nadia M.; Pierre, Fabrice H.F.; Corpet, Denis E. (2011). "Heme Iron from Meat and Risk of Colorectal Cancer: A Meta-analysis and a Review of the Mechanisms Involved". Cancer Prevention Research 4 (2): 177–184. doi:10.1158/1940-6207.CAPR-10-0113. PMID 21209396. https://cancerpreventionresearch.aacrjournals.org/content/4/2/177. 
  4. ↑ Bastide, Nadia M.; Chenni, Fatima; Audebert, Marc; Santarelli, Raphaelle L.; Taché, Sylviane; Naud, Nathalie; Baradat, Maryse; Jouanin, Isabelle et al. (2015). "A Central Role for Heme Iron in Colon Carcinogenesis Associated with Red Meat Intake". Cancer Research 75 (5): 870–879. doi:10.1158/0008-5472.CAN-14-2554. PMID 25592152. https://cancerres.aacrjournals.org/content/75/5/870. 
  5. ↑ Jakszyn, P; Gonzalez, CA (2006). "Nitrosamine and related food intake and gastric and oesophageal cancer risk: A systematic review of the epidemiological evidence". World Journal of Gastroenterology 12 (27): 4296–4303. doi:10.3748/wjg.v12.i27.4296. PMID 16865769. 
  6. ↑ Joyce I. Boye; Yves Arcand (2012-01-10). Green Technologies in Food Production and Processing. Springer Science & Business Media. p. 573. ISBN 978-1-4614-1586-2. https://books.google.com/books?id=k617lqxxDSgC&pg=PA573. 
  7. ↑ Lee, L; Archer, MC; Bruce, WR (October 1981). "Absence of volatile nitrosamines in human feces". Cancer Res. 41 (10): 3992–4. PMID 7285009. 
  8. ↑ Kuhnle, GG et al. (October 2007). "Diet-induced endogenous formation of nitroso compounds in the GI tract". Free Radic. Biol. Med. 43 (7): 1040–7. doi:10.1016/j.freeradbiomed.2007.03.011. PMID 17761300. 
  9. ↑ Mirvish, SS; Wallcave, L; Eagen, M; Shubik, P (July 1972). "Ascorbate–nitrite reaction: possible means of blocking the formation of carcinogenic N-nitroso compounds". Science 177 (4043): 65–8. doi:10.1126/science.177.4043.65. PMID 5041776. Bibcode: 1972Sci...177...65M. 
  10. ↑ Mirvish, SS (October 1986). "Effects of vitamins C and E on N-nitroso compound formation, carcinogenesis, and cancer". Cancer 58 (8 Suppl): 1842–50. doi:10.1002/1097-0142(19861015)58:8+<1842::aid-cncr2820581410>3.0.co;2-#. PMID 3756808. 
  11. ↑ "Inhibition of nitrosamine formation by ascorbic acid". The American Journal of Clinical Nutrition 53 (1 Suppl): 247S–250S. 1991. doi:10.1111/j.1749-6632.1987.tb23774.x. PMID 1985394. Bibcode: 1987NYASA.498..354T. http://www.ajcn.org/cgi/pmidlookup?view=long&pmid=1985394. Retrieved 2015-06-06. "Evidence now exists that ascorbic acid is a limiting factor in nitrosation reactions in people.". 
  12. ↑ Combet, E.; Paterson, S; Iijima, K; Winter, J; Mullen, W; Crozier, A; Preston, T; McColl, K. E. (2007). "Fat transforms ascorbic acid from inhibiting to promoting acid-catalysed N-nitrosation". Gut 56 (12): 1678–1684. doi:10.1136/gut.2007.128587. PMID 17785370. 
  13. ↑ Combet, E; El Mesmari, A; Preston, T; Crozier, A; McColl, K. E. (2010). "Dietary phenolic acids and ascorbic acid: Influence on acid-catalyzed nitrosative chemistry in the presence and absence of lipids". Free Radical Biology and Medicine 48 (6): 763–771. doi:10.1016/j.freeradbiomed.2009.12.011. PMID 20026204. 



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