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      Thermal processing food-related toxicants: a review

      1 , 1
      Critical Reviews in Food Science and Nutrition
      Informa UK Limited

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          Abstract

          <p class="first" id="d5258204e57">Heterocyclic aromatic amines, acrylamide, 5-hydroxymethylfurfural, furan, polycyclic aromatic hydrocarbons, nitrosamines, acrolein, chloropropanols and chloroesters are generated toxicants formed in some foodstuffs, mainly starchy and protein-rich food during thermal treatment such as frying, roasting and baking. The formation of these chemical compounds is associated with development of aromas, colors and flavors. One of the challenges facing the food industry today is to minimize these toxicants without adversely affecting the positive attributes of thermal processing. To achieve this objective, it is essential to have a detailed understanding of the mechanism of formation of these toxicants in processed foods. All reviewed toxicants in that paper are classified as probable, possible or potential human carcinogens and have been proven to be carcinogenic in animal studies. The purpose of that review is to summarize some of the most frequent occurring heat-generated food toxicants during conventional heating, their metabolism and carcinogenicity. Moreover, conventional and microwave heating were also compared as two different heat treatment methods, especially how they change food chemical composition and which thermal food toxicants are formed during specific method. </p>

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          Most cited references108

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          A review on polycyclic aromatic hydrocarbons: Source, environmental impact, effect on human health and remediation

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            Acrolein: sources, metabolism, and biomolecular interactions relevant to human health and disease.

            Acrolein (2-propenal) is ubiquitously present in (cooked) foods and in the environment. It is formed from carbohydrates, vegetable oils and animal fats, amino acids during heating of foods, and by combustion of petroleum fuels and biodiesel. Chemical reactions responsible for release of acrolein include heat-induced dehydration of glycerol, retro-aldol cleavage of dehydrated carbohydrates, lipid peroxidation of polyunsaturated fatty acids, and Strecker degradation of methionine and threonine. Smoking of tobacco products equals or exceeds the total human exposure to acrolein from all other sources. The main endogenous sources of acrolein are myeloperoxidase-mediated degradation of threonine and amine oxidase-mediated degradation of spermine and spermidine, which may constitute a significant source of acrolein in situations of oxidative stress and inflammation. Acrolein is metabolized by conjugation with glutathione and excreted in the urine as mercapturic acid metabolites. Acrolein forms Michael adducts with ascorbic acid in vitro, but the biological relevance of this reaction is not clear. The biological effects of acrolein are a consequence of its reactivity towards biological nucleophiles such as guanine in DNA and cysteine, lysine, histidine, and arginine residues in critical regions of nuclear factors, proteases, and other proteins. Acrolein adduction disrupts the function of these biomacromolecules which may result in mutations, altered gene transcription, and modulation of apoptosis.
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              Heterocyclic amines: Mutagens/carcinogens produced during cooking of meat and fish.

              Research leading to the discovery of a series of mutagenic and carcinogenic heterocyclic amines (HCAs) was inspired by the idea that smoke produced during cooking of food, especially meat or fish, might be carcinogenic. More than ten kinds of HCAs, actually produced by cooking or heating of meat or fish, have now been isolated and their structures determined, most being previously unregistered compounds. They are highly mutagenic towards Salmonella typhimurium in the presence of S9 mix and are also mutagenic in vitro and in vivo toward mammalian cells. HCAs have now been chemically synthesized in quantity and subjected to long-term animal testing. When HCAs were fed in the diet, rodents developed cancers in many organs, including the colon, breast and prostate, and one HCA produced hepatomas in monkeys. The lesions exhibited alteration in genes including Apc, beta-catenin and Ha-ras, and these changes provide clues to the induction mechanisms. The HCAs are oxidized to hydroxyamino derivatives by cytochrome P450s, and further converted to ester forms by acetyltransferase and sulfotransferase. Eventually, they produce DNA adducts through the formation of N-C bonds at guanine bases. There are HCA-sensitive and resistant strains of rodents and a search for the responsible genes is now under way. While the content of HCAs in dishes consumed in ordinary life is low and not sufficient in itself to explain human cancer, the coexistence of many other mutagens/carcinogens of either autobiotic or xenobiotic type and the possibility that HCAs induce genomic instability and heightened sensitivity to tumor promoters suggest that avoidance of exposure to HCAs or reduction of HCAs' biological effects as far as possible are to be highly recommended. Usage of microwave ovens for cooking and supplementation of the diet, for example with soy-isoflavones, which have been found to suppress the occurrence of HCA-induced breast cancers, should be encouraged. Advice to the general public about how to reduce the carcinogenic load imposed by HCAs would be an important contribution to cancer prevention.
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                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
                December 16 2019
                October 12 2018
                December 16 2019
                : 59
                : 22
                : 3579-3596
                Affiliations
                [1 ] Institute of Fermentation Technology and Microbiology, Lodz University of Technology, Lodz, Poland
                Article
                10.1080/10408398.2018.1500440
                30311772
                c486f761-0dbd-4c32-95ba-5de109a6eb99
                © 2019
                History

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