10
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: not found
      • Article: not found

      Mechanisms Linking Colorectal Cancer to the Consumption of (Processed) Red Meat: A Review

      , , ,
      Critical Reviews in Food Science and Nutrition
      Informa UK Limited

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Colorectal cancer (CRC) is the third most commonly diagnosed cancer in the world. The vast majority of CRC cases have been linked to environmental causes rather than to heritable genetic changes. Over the last decades, epidemiological evidence linking the consumption of red and, more convincingly, of processed red meat to CRC has accumulated. In parallel, hypotheses on carcinogenic mechanisms underlying an association between CRC and the intake of red and processed red meat have been proposed and investigated in biological studies. The hypotheses that have received most attention until now include (1) the presence of polycyclic aromatic hydrocarbons and heterocyclic aromatic amines, two groups of compounds recognized as carcinogenic, (2) the enhancing effect of (nitrosyl)heme on the formation of carcinogenic N-nitroso compounds and lipid peroxidation. However, none of these hypotheses completely explains the link between red and processed red meat intake and the CRC risk. Consequently, scientists have proposed additional mechanisms or refined their hypotheses. This review first briefly summarizes the development of CRC followed by an in-depth overview and critical discussion of the different potential carcinogenic mechanisms underlying the increased CRC risk associated with the consumption of red and processed red meat.

          Related collections

          Most cited references160

          • Record: found
          • Abstract: found
          • Article: not found

          Radical causes of cancer.

          Free radicals are ubiquitous in our body and are generated by normal physiological processes, including aerobic metabolism and inflammatory responses, to eliminate invading pathogenic microorganisms. Because free radicals can also inflict cellular damage, several defences have evolved both to protect our cells from radicals--such as antioxidant scavengers and enzymes--and to repair DNA damage. Understanding the association between chronic inflammation and cancer provides insights into the molecular mechanisms involved. In particular, we highlight the interaction between nitric oxide and p53 as a crucial pathway in inflammatory-mediated carcinogenesis.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            The use and control of nitrate and nitrite for the processing of meat products.

            Nitrate and nitrite are used for the purpose of curing meat products. In most countries the use of both substances, usually added as potassium or sodium salts, is limited. Either the ingoing or the residual amounts are regulated by laws. The effective substance is nitrite acting primarily as an inhibitor for some microorganisms. Nitrite added to a batter of meat is partially oxidized to nitrate by sequestering oxygen - thus it acts as an antioxidant - a part of nitrite is bound to myoglobin, forming the heat stable NO-myoglobin, a part is bound to proteins or other substances in meat. Nitrate may be reduced to nitrite in raw meat products by microorganisms. As oxidation and reduction may occur the concentrations of nitrite plus nitrate in a product has to be controlled and measured especially if the residual amounts are regulated. This sum of both compounds is important for the human body. Intake of nitrate with food leads to its absorption over the digestive tract into the blood. In the oral cavity nitrate appears again where it is reduced to nitrite. With the saliva the nitrite is mixed with food, having the same effect as nitrite in a batter (inhibiting growth of some pathogenic microorganisms) and swallowed. In the stomach nitrite can eventually form carcinogenic nitrosamines in the acidic environment.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Role of N-nitroso compounds (NOC) and N-nitrosation in etiology of gastric, esophageal, nasopharyngeal and bladder cancer and contribution to cancer of known exposures to NOC.

              The questions of whether and how N-nitroso compounds (NOC) may be inducing cancer in humans are discussed. The principal subjects covered include nitrite-derived alkylating agents that are not NOC, reasons for the wide tissue specificity of carcinogenesis by NOC, the acute toxicity of nitrosamines in humans, mechanisms of in vivo formation of NOC by chemical and bacterial nitrosation in the stomach and via nitric oxide (NO) formation during inflammation, studies on nitrite esters, use of the nitrosoproline test to follow human gastric nitrosation, correlations of nitrate in food and water with in vivo nitrosation and the inhibition of gastric nitrosation by vitamin C and polyphenols. Evidence that specific cancers are caused by NOC is reviewed for cancer of the stomach, esophagus, nasopharynx, urinary bladder in bilharzia and colon. I review the occurrence of nitrosamines in tobacco products, nitrite-cured meat (which might be linked with childhood leukemia and brain cancer) and other foods, and in drugs and industrial situations. Finally, I discuss clues from mutations in ras and p53 genes in human tumors about whether NOC are etiologic agents and draw some general conclusions.
                Bookmark

                Author and article information

                Journal
                Critical Reviews in Food Science and Nutrition
                Critical Reviews in Food Science and Nutrition
                Informa UK Limited
                1040-8398
                1549-7852
                June 05 2015
                December 09 2016
                May 15 2015
                December 09 2016
                : 56
                : 16
                : 2747-2766
                Article
                10.1080/10408398.2013.873886
                25975275
                52e03f94-87a6-4380-89c6-59e35afbaa03
                © 2016
                History

                Comments

                Comment on this article