Meat, Meat cooking methods and preservation, and risk for colorectal carcinoma

Nutritional Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, Maryland, USA.
Cancer Research (Impact Factor: 9.33). 10/2005; 65(17):8034-41. DOI: 10.1158/0008-5472.CAN-04-3429
Source: PubMed

ABSTRACT Cooking meat at high temperatures produces heterocyclic amines (HCAs) and polycyclic aromatic hydrocarbons (PAHs). Processed meats contain N-nitroso compounds. Meat intake may increase cancer risk as HCAs, PAHs, and N-nitroso compounds are carcinogenic in animal models. We investigated meat, processed meat, HCAs, and the PAH benzo(a)pyrene and the risk of colorectal adenoma in 3,696 left-sided (descending and sigmoid colon and rectum) adenoma cases and 34,817 endoscopy-negative controls. Dietary intake was assessed using a 137-item food frequency questionnaire, with additional questions on meats and meat cooking practices. The questionnaire was linked to a previously developed database to determine exposure to HCAs and PAHs. Intake of red meat, with known doneness/cooking methods, was associated with an increased risk of adenoma in the descending and sigmoid colon [odds ratio (OR), 1.26; 95% confidence interval (95% CI), 1.05-1.50 comparing extreme quintiles of intake] but not rectal adenoma. Well-done red meat was associated with increased risk of colorectal adenoma (OR, 1.21; 95% CI, 1.06-1.37). Increased risks for adenoma of the descending colon and sigmoid colon were observed for the two HCAs: 2-amino-3,8-dimethylimidazo[4,5]quinoxaline and 2-amino-1-methyl-6-phenylimidazo[4,5]pyridine (OR, 1.18; 95% CI, 1.01-1.38 and OR, 1.17, 95% CI, 1.01-1.35, respectively) as well as benzo(a)pyrene (OR, 1.18; 95% CI, 1.02-1.35). Greater intake of bacon and sausage was associated with increased colorectal adenoma risk (OR, 1.14; 95% CI, 1.00-1.30); however, total intake of processed meat was not (OR, 1.04; 95% CI, 0.90-1.19). Our study of screening-detected colorectal adenomas shows that red meat and meat cooked at high temperatures are associated with an increased risk of colorectal adenoma.

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    • "family , including CYP1A1 and 1B1 , can activate dietary pro - carcinogens such as heterocyclic amines and polycyclic aromatic hydrocarbons , which have been associated with colorectal cancer ( Ito et al , 1991 ; Crofts et al , 1997 ; Barrett et al , 2003 ; Boyce et al , 2004 ; Sinha et al , 2005 ; Nothlings et al , 2009 ) , and the expression of CYP450 enzymes in tissues that are targets for xenobiotic genotoxicity implies a potential for in situ activation . CYP450s , in particular CYP2E1 , can also metabolise several drugs resulting in either inhibition or activation , and thus have an important role in drug bioavailability ( Koop , 1992 ) . "
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    ABSTRACT: Background: The pro-inflammatory cytokine interleukin-6 (IL6) promotes colorectal cancer (CRC) development. It is also known to regulate cytochrome P450 (CYP450) enzymes, which are involved in CRC tumour initiation and promotion via activation of chemical carcinogens. Here, IL6 regulation of CYP450 expression was investigated in CRC. Methods: The effect of IL6 on CYP 1A1, 1B1 and 2E1 expression was determined in vitro using CRC cell lines HCT116 and SW480, and CYP450 expression was determined by immunohistochemistry in CRC tissues previously shown to have increased levels of IL6. Results: In mechanistic studies, IL6 treatment significantly induced CYP1B1 and CYP2E1, but not CYP1A1, gene expression in HCT116 and SW480 cells. CYP2E1 expression regulation occurred via a transcriptional mechanism involving STAT3. For CYP1B1 regulation, IL6 downregulated the CYP1B1-targeting microRNA miR27b through a mechanism involving DNA methylation. In clinical samples, the expression of CYP1B1 and CYP2E1, but not CYP1A1, was significantly increased in malignant tissue overexpressing IL6 compared with matched adjacent normal tissue. Conclusions: Colonic inflammation with the presence of IL6 associated with neoplastic tissue can alter metabolic competency of epithelial cells by manipulating CYP2E1 and CYP1B1 expression through transcriptional and epigenetic mechanisms. This can lead to increased activation of dietary carcinogens and DNA damage, thus promoting colorectal carcinogenesis.
    British Journal of Cancer 10/2014; 111(12):2287-96. DOI:10.1038/bjc.2014.540 · 4.84 Impact Factor
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    • "The human activity, including fossil fuel combustion and industrial processing, is the primary source of PAHs contamination in the environment, but they can be also generated by natural phenomena, such as forest fires. Recent studies have shown that high level of PAHs are found in meat cooked at high temperatures (Sinha et al., 2005) and in smoked fish (Stolyhwo and Sikorski, 2005). These ubiquitous environmental contaminants have raised considerable misgivings, because many PAHs, besides the negative impacts on the surrounding ecosystem, have been shown to have potential mutagenic, carcinogenic and teratogenic activities after being metabolized (Bofetta et al., 1997; Ismert et al., 2002), causing adverse health effects; their hydrophilic character allows them to enter cells easily, inducing the metabolic system that will transform these molecules (Ismert et al., 2002). "
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    ABSTRACT: A combined experimental and computational study was developed to evaluate and understand the energetics and reactivity of formyl and methoxy α-naphthalene derivatives. Static bomb combustion calorimetry and the Calvet microcalorimetry were the experimental techniques used to determine the standard (p(o)=0.1MPa) molar enthalpies of formation, in the liquid phase, ΔfHm(o)(l), and of vaporization, Δl(g)Hm(o), at T=298.15K, respectively, of the two liquid naphthalene derivatives. Those experimental values were used to derive the values of the experimental standard molar enthalpies of formation, in the gaseous phase, ΔfHm(o)(g), of 1-methoxynaphthalene, (-3.0±3.1)kJmol(-1), and of 1-formylnaphthalene, (36.3±4.1)kJmol(-1). High-level quantum chemical calculations at the composite G3(MP2)//B3LYP level were performed to estimate the values of the ΔfHm(o)(g) of the two compounds studied resulting in values in very good agreement with experimental ones. Natural bond orbital (NBO) calculations were also performed to determine more about the structure and reactivity of this class of compounds.
    Chemosphere 01/2014; 107. DOI:10.1016/j.chemosphere.2013.12.044 · 3.34 Impact Factor
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    • "Polycyclic aromatic hydrocarbons (PAHs) have long been recognized as one group of global pollutants found in complex mixtures that mainly originate from incomplete combustion related to numerous anthropogenic sources such as petroleum fuels, refining industries, and production processes (Boonyatumanond et al. 2006, Hylland 2006, Marie et al. 2009, Nelson 2009, Shen et al. 2011b, Simoneit et al. 2005, Timoney and Lee 2011, Yang et al. 1998). Moreover, PAHs are also found in various heating fumes and cigarette smoke etc. (Castro et al. 2011, Ohura et al. 2003, Phillips 1999, Sinha et al. 2005, Wretling et al. 2010). PAHs belong to a class of several hundred individual chemicals that contains at least two fused benzenoid rings. "
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    ABSTRACT: Polycyclic aromatic hydrocarbons (PAHs) are well-known carcinogens to humans and ecotoxicological effects have been shown in several studies. However, PAHs can also be oxidized into more water soluble-oxygenated metabolites (Oxy-PAHs). The first purpose of the present project was to (1) assess the effects of a mixture containing three parent PAHs: anthracene, benz[a]anthracene, and benzo[a]pyrene versus a mixture of their oxygenated metabolites, namely: anthracene-9,10-dione, benz[a]anthracene-7,12-dione, and 9,10-dihydrobenzo[a]pyrene-7-(8H)-one on the hepatic fatty acid β-oxidation in chicken embryos (Gallus gallus domesticus) exposed in ovo. The second and also main purpose of the project was to (2) assess the effects of the parent PAHs versus their oxy-PAHs analogues when injected individually, followed by (3) additional testing of the individual oxy-PAHs. The hepatic β-oxidation was measured using a tritium release assay with [9,10-(3)H]-palmitic acid (16:0) as substrate. The result from the first part (1) showed reduced hepatic β-oxidation after exposure in ovo to a mixture of three PAHs, however, increased after exposure to the mixture of three oxy-PAHs compared to control. The result from the second part (2) and also the follow-up experiment (3) showed that 9,10-dihydrobenzo[a]pyrene-7-(8H)-one was the causative oxy-PAH. The implication of this finding on the risk assessment of PAH metabolite exposure in avian wildlife remains to be determined. To the best of our knowledge, no similar studies have been reported.
    Environmental Science and Pollution Research 01/2014; 21(9). DOI:10.1007/s11356-013-2471-6 · 2.83 Impact Factor
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