scholarly journals An arabinoxylan-rich fraction from wheat enhances caecal fermentation and protects colonocyte DNA against diet-induced damage in pigs

2011 ◽  
Vol 107 (9) ◽  
pp. 1274-1282 ◽  
Author(s):  
Damien P. Belobrajdic ◽  
Anthony R. Bird ◽  
Michael A. Conlon ◽  
Barbara A. Williams ◽  
Seungha Kang ◽  
...  
Keyword(s):  
Dna Damage ◽  
Large Bowel ◽  
Dietary Fibre ◽  
Epidemiological Data ◽  
Red Meat ◽  
Processed Meat ◽  
Microbial Composition ◽  
Clostridial Cluster ◽  
Carbohydrate Fermentation ◽  
Dna Strand

Population studies show that greater red and processed meat consumption increases colorectal cancer risk, whereas dietary fibre is protective. In rats, resistant starches (a dietary fibre component) oppose colonocyte DNA strand breaks induced by high red meat diets, consistent with epidemiological data. Protection appears to be through SCFA, particularly butyrate, produced by large bowel carbohydrate fermentation. Arabinoxylans are important wheat fibre components and stimulate large bowel carbohydrate SCFA production. The present study aimed to determine whether an arabinoxylan-rich fraction (AXRF) from wheat protected colonocytes from DNA damage and changed colonic microbial composition in pigs fed with a diet high (30 %) in cooked red meat for 4 weeks. AXRF was primarily fermented in the caecum, as indicated by higher tissue and digesta weights and higher caecal (but not colonic) acetate, propionate and total SCFA concentrations. Protein fermentation product concentrations (caecalp-cresol and mid- and distal colonic phenol) were lower in pigs fed with AXRF. Colonocyte DNA damage was lower in pigs fed with AXRF. The microbial profiles of mid-colonic mucosa and adjacent digesta showed that bacteria affiliating withPrevotellaspp. and Clostridial cluster IV were more abundant in both the mucosa and digesta fractions of pigs fed with AXRF. These data suggest that, although AXRF was primarily fermented in the caecum, DNA damage was reduced in the large bowel, occurring in conjunction with lower phenol concentrations and altered microbial populations. Further studies to determine the relationships between these changes and the lowering of colonocyte DNA damage are warranted.

scholarly journals The associations of major foods and fibre with risk of ischaemic and haemorrhagic stroke: results from the prospective EPIC study.

2020 ◽  
Vol 79 (OCE2) ◽  
Author(s):  
Tammy Y.N. Tong ◽  
Paul N. Appleby ◽  
Timothy J. Key ◽  
Aurora Perez-Cornago
Keyword(s):  
Ischaemic Stroke ◽  
Dietary Fibre ◽  
Positive Association ◽  
Haemorrhagic Stroke ◽  
Red Meat ◽  
Fruit And Vegetables ◽  
Processed Meat ◽  
Egg Consumption ◽  
Egg Plant ◽  
Red And Processed Meat

AbstractIntroductionThe evidence of associations between individual foods and dietary fibre with subtypes of stroke (ischaemic and haemorrhagic) is not conclusive. We aimed to investigate this in a large prospective cohort.Materials and methodsWe analysed data on 418,329 men and women from the European Prospective Investigation into Cancer and Nutrition (EPIC) study. Consumption of various animal-sourced foods (red and processed meat, poultry, fish, dairy, egg), plant-sourced foods (fruit and vegetables, legumes, nuts and seeds) and dietary fibre was assessed using validated country-specific questionnaires, calibrated with 24-hour recalls. Using multivariable Cox regressions adjusted for energy intake and socio-demographic, lifestyle and physiological confounders, we estimated hazard ratios of fatal and non-fatal ischaemic, haemorrhagic and total (i.e. ischaemic, haemorrhagic and unspecified) stroke associated with calibrated increment differences in consumption of each food or dietary fibre.ResultsOver an average of 12.7 years of follow-up, we observed 4281 cases of ischaemic stroke, 1430 cases of haemorrhagic stroke, and 7378 cases of total stroke. For ischaemic stroke, lower risks were observed with higher consumption of fruit and vegetables (hazard ratio (HR); 95% confidence interval (CI) for per 200g/d of calibrated intake, 0.87; 0.82–0.93) and dietary fibre (per 10g/d, HR 0.77; 95% CI 0.69–0.86) (p-trend < 0.001 for both); more modest inverse associations were also observed for milk (per 200g/d, HR 0.95; 95% CI 0.91–0.99, p-trend = 0.02), yogurt (per 100g/d, HR 0.91; 95% CI 0.85–0.97, p-trend = 0.004) and cheese (per 30g/d, HR 0.88; 95% CI 0.81–0.97, p-trend = 0.008), while a modest positive association was observed with higher red meat consumption (per 50g/d, HR 1.14; 95% CI 1.02–1.27, p-trend = 0.02). For haemorrhagic stroke, higher risk was associated with higher egg consumption (per 20g/d, HR 1.25; 95% CI 1.09–1.43, p-trend = 0.002). For total stroke, associations were consistent with those of both subtypes; we observed inverse associations for fruit and vegetables (HR 0.89, 95% CI 0.85–0.93), dietary fibre (HR 0.80, 95% CI 0.74–0.86), yogurt (HR 0.91, 95% CI 0.87–0.96), cheese (HR 0.88, 95% CI 0.82–0.94), and positive associations for red and processed meat (HR 1.18, 95% CI 1.05–1.33) and egg (HR 1.07, 95% CI 1.01–1.14).DiscussionTo conclude, risk of ischaemic stroke was inversely associated with consumption of fruit and vegetables, dietary fibre and dairy foods, and positively associated with red meat, while risk of haemorrhagic stroke was positively associated with egg consumption. Causality of the associations cannot be determined in this observational study.

scholarly journals Towards refining WCRF/AICR cancer prevention recommendations for red and processed meat intake: Insights from Alberta’s Tomorrow Project cohort

2021 ◽  
pp. 1-38
Author(s):  
Ala Al Rajabi ◽  
Geraldine Lo Siou ◽  
Alianu K. Akawung ◽  
Kathryn L McDonald ◽  
Tiffany R. Price ◽  
...  
Keyword(s):  
Cancer Prevention ◽  
Proportional Hazards ◽  
Red Meat ◽  
Cox Proportional Hazards ◽  
Processed Meat ◽  
Carcinogenic Effect ◽  
Meat Intake ◽  
Increased Risk ◽  
Red Meats ◽  
Red And Processed Meat

ABSTRACT Current cancer prevention recommendations advise limiting red meat intake to <500g/week and avoiding consumption of processed meat, but do not differentiate the source of processed meat. We examined the associations of processed meat derived from red vs. non-red meats with cancer risk in a prospective cohort of 26,218 adults who reported dietary intake using the Canadian Diet History Questionnaire. Incidence of cancer was obtained through data linkage with Alberta Cancer Registry with median (IQR) follow-up of 13.3 (5.1) years. Multivariable Cox proportional hazards regression models were adjusted for covariates and stratified by age and gender. The median (IQR) consumption (g/week) of red meat, processed meat from red meat and processed meat from non-red meat were 267.9 (269.9), 53.6 (83.3), and 11.9 (31.8), respectively. High intakes (4th Quartile) of processed meat from red meat was associated with increased risk of gastro-intestinal cancer Adjusted Hazard Ratio (AHR) (95% CI): 1.68 (1.09 – 2.57) and colorectal cancers AHR (95% CI): 1.90 (1.12 – 3.22), respectively in women. No statistically significant associations were observed for intakes of red meat or processed meat from non-red meat. Results suggests that the carcinogenic effect associated with processed meat intake may be limited to processed meat derived from red meats. The findings provide preliminary evidence toward refining cancer prevention recommendations for red and processed meat intake.

scholarly journals Associations of Processed Meat, Unprocessed Red Meat, Poultry, or Fish Intake With Incident Cardiovascular Disease and All-Cause Mortality

2020 ◽  
Vol 180 (4) ◽  
pp. 503 ◽  
Author(s):  
Victor W. Zhong ◽  
Linda Van Horn ◽  
Philip Greenland ◽  
Mercedes R. Carnethon ◽  
Hongyan Ning ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Red Meat ◽  
Fish Intake ◽  
Processed Meat ◽  
All Cause Mortality ◽  
Incident Cardiovascular Disease

scholarly journals Synthesis and in vitro characterization of the genotoxic, mutagenic and cell-transforming potential of nitrosylated heme

2020 ◽  
Vol 94 (11) ◽  
pp. 3911-3927 ◽  
Author(s):  
Tina Kostka ◽  
Jörg Fohrer ◽  
Claudia Guigas ◽  
Karlis Briviba ◽  
Nina Seiwert ◽  
...  
Keyword(s):  
Cell Transformation ◽  
Malignant Cell ◽  
Red Meat ◽  
Colorectal Carcinogenesis ◽  
In Vivo Studies ◽  
Processed Meat ◽  
Cell Transforming ◽  
Malignant Cell Transformation

Abstract Data from epidemiological studies suggest that consumption of red and processed meat is a factor contributing to colorectal carcinogenesis. Red meat contains high amounts of heme, which in turn can be converted to its nitrosylated form, NO-heme, when adding nitrite-containing curing salt to meat. NO-heme might contribute to colorectal cancer formation by causing gene mutations and could thereby be responsible for the association of (processed) red meat consumption with intestinal cancer. Up to now, neither in vitro nor in vivo studies characterizing the mutagenic and cell transforming potential of NO-heme have been published due to the fact that the pure compound is not readily available. Therefore, in the present study, an already existing synthesis protocol was modified to yield, for the first time, purified NO-heme. Thereafter, newly synthesized NO-heme was chemically characterized and used in various in vitro approaches at dietary concentrations to determine whether it can lead to DNA damage and malignant cell transformation. While NO-heme led to a significant dose-dependent increase in the number of DNA strand breaks in the comet assay and was mutagenic in the HPRT assay, this compound tested negative in the Ames test and failed to induce malignant cell transformation in the BALB/c 3T3 cell transformation assay. Interestingly, the non-nitrosylated heme control showed similar effects, but was additionally able to induce malignant transformation in BALB/c 3T3 murine fibroblasts. Taken together, these results suggest that it is the heme molecule rather than the NO moiety which is involved in driving red meat-associated carcinogenesis.

Red meat consumption and type 2 diabetes mellitus risk

2015 ◽  
Vol 45 (4) ◽  
pp. 524-541
Author(s):  
Emma Derbyshire ◽  
Carrie Ruxton
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Clinical Studies ◽  
Meat Consumption ◽  
Red Meat ◽  
Review Literature ◽  
Processed Meat ◽  
Content Type

Purpose – This review aims to evaluate and review literature published in the area of rising concerns that red meat consumption may be associated with risk of type 2 diabetes mellitus (T2DM), although there have been discrepancies between study findings, and put the findings into context. Design/methodology/approach – Using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, a systematic literature review was undertaken to locate and summarise relevant studies which included epidemiological and clinical studies published between 2004 and 2014. Findings – A total of 23 studies were found, with 21 epidemiological and two clinical studies meeting the criteria. Overall, the totality of the evidence indicates that while processed meat consumption appears to be associated with T2DM risk, the effect is much weaker for red meat, with some associations attenuated after controlling for body weight parameters. Where studies have considered high intakes in relation to T2DM risk, meat intake has tended to exceed 600 g per week. Therefore, keeping red meat intakes within recommended guidelines of no more than 500 g per week, while opting for lean cuts or trimming fat, would seem to be an evidence-based response. Research limitations/implications – The majority of studies conducted to date have been observational cohorts which cannot determine cause and effect. Most of these used food frequency questionnaires which are known to be subject to misclassification errors (Brown, 2006). Clearly, more randomised controlled trials are needed to establish whether red meat consumption impacts on markers of glucose control. Until then, conclusions can only be viewed as speculative. Originality/value – This paper provides an up-to-date systematic review of the literature, looking at inter-relationships between red meat consumption and T2DM risk.

scholarly journals Repair of DNA Strand Breaks by the Overlapping Functions of Lesion-Specific and Non-Lesion-Specific DNA 3′ Phosphatases

2001 ◽  
Vol 21 (21) ◽  
pp. 7191-7198 ◽  
Author(s):  
John R. Vance ◽  
Thomas E. Wilson
Keyword(s):  
Dna Damage ◽  
Oxidative Dna Damage ◽  
Synthetic Lethality ◽  
Dna Strand Breaks ◽  
Triple Mutant ◽  
Phosphatase Domain ◽  
Strand Breaks ◽  
Alternative Pathways ◽  
Processing Enzymes ◽  
Dna Strand

ABSTRACT In Saccharomyces cerevisiae, the apurinic/apyrimidinic (AP) endonucleases Apn1 and Apn2 act as alternative pathways for the removal of various 3′-terminal blocking lesions from DNA strand breaks and in the repair of abasic sites, which both result from oxidative DNA damage. Here we demonstrate that Tpp1, a homologue of the 3′ phosphatase domain of polynucleotide kinase, is a third member of this group of redundant 3′ processing enzymes. Unlike Apn1 and Apn2, Tpp1 is specific for the removal of 3′ phosphates at strand breaks and does not possess more general 3′ phosphodiesterase, exonuclease, or AP endonuclease activities. Deletion ofTPP1 in an apn1 apn2 mutant background dramatically increased the sensitivity of the double mutant to DNA damage caused by H2O2 and bleomycin but not to damage caused by methyl methanesulfonate. The triple mutant was also deficient in the repair of 3′ phosphate lesions left by Tdp1-mediated cleavage of camptothecin-stabilized Top1-DNA covalent complexes. Finally, the tpp1 apn1 apn2 triple mutation displayed synthetic lethality in combination with rad52, possibly implicating postreplication repair in the removal of unrepaired 3′-terminal lesions resulting from endogenous damage. Taken together, these results demonstrate a clear role for the lesion-specific enzyme, Tpp1, in the repair of a subset of DNA strand breaks.

Factors which affect DNA strand breakage in human leukocytes exposed to a tumor promoter, phorbol myristate acetate

1982 ◽  
Vol 60 (11) ◽  
pp. 1359-1366 ◽  
Author(s):  
H. C. Birnboim
Keyword(s):  
Hydrogen Peroxide ◽  
Dna Damage ◽  
Phorbol Myristate Acetate ◽  
Respiratory Burst ◽  
Superoxide Anion ◽  
Tumor Promoter ◽  
Myristate Acetate ◽  
Strand Breakage ◽  
Dna Strand ◽  
Dna Strand Breakage

We have recently reported that phorbol myristate acetate (PMA) induces extensive DNA strand break damage in human peripheral blood leukocytes. The mechanism of action involves superoxide anion and hydrogen peroxide which are generated by phagocytes during the "respiratory burst." In this report, we describe the effect of various inhibitors and scavengers on PMA-induced DNA damage. Azide and cyanide greatly increased the level of damage; sulfhydryl compounds (glutathione, cysteine, and cysteamine) and ascorbate markedly decreased the level of damage. Hydroxyl radical scavengers such as dimethyl sulfoxide (DMSO) and glycerol also decreased the level of damage but apparently did so by inhibiting the respiratory burst. Diethyldithiocarbamate (DDC) increased the level of DNA damage at low concentrations (<1 mM), but decreased DNA damage at ≥1 mM. The results are consistent with a mechanism involving superoxide anion and hydrogen peroxide, but the precise reaction (free radical or enzymatic) responsible for DNA strand breakage has not been determined. The PMA-stimulated phagocyte is an interesting model system for looking at "active oxygen" mediated DNA damage and factors which influence it.

scholarly journals Engineered Nanoparticles Induce DNA Damage in Primary Human Skin Cells, Even at Low Doses

Nano LIFE ◽  
2014 ◽  
Vol 04 (01) ◽  
pp. 1440001 ◽  
Author(s):  
Amelia A. Romoser ◽  
Michael F. Criscitiello ◽  
Christie M. Sayes
Keyword(s):  
Dna Damage ◽  
Stress Protein ◽  
Dermal Fibroblasts ◽  
Engineered Nanoparticles ◽  
Ros Generation ◽  
Heme Oxygenase 1 ◽  
Dna Double Strand Breaks ◽  
Biological Reduction ◽  
Strand Breaks ◽  
Dna Strand

It is well documented that various particulate matter — either incidental or engineered — are known to generate reactive oxygen species (ROS) in living cells. In circumstances where these reactive species are generated, antioxidant production is often increased. This balance in the biological reduction/oxidation (a.k.a. redox) state within the cell has not been thoroughly studied in exposures involving engineered nanoparticles. However, nanoparticle exposure has been postulated to induce a DNA damage cascade. In this study, we examined primary human dermal fibroblasts (HDF) exposed to three different, but commonly used engineered nanoparticles (i.e., cerium dioxide ( CeO 2), titanium dioxide ( TiO 2) and zinc oxide ( ZnO )) in an attempt to determine the potential DNA damaging effects through the analysis of ROS generation, relevant protein upregulation response and single and double DNA strand breaks. Cell death was most elevated with exposure to ZnO , followed by TiO 2 and CeO 2. ROS generation was measured at 1 h, 6 h and 24 h after exposure to particles via a cell-based DCFH-DA (2′, 7′-dichlorfluorescein-diacetate) assay and indicated that ZnO generated the most significant amount of ROS. ZnO also caused upregulation of oxidative stress protein, heme oxygenase-1 and phosphorylation of p38; whereas CeO 2 caused upregulation of superoxide dismutase. Results from the comet assay indicated that ZnO triggered significant DNA damage in cells at relatively low dosing concentrations (20 ppm). Immunocytochemistry with ZnO -treated cells revealed notable DNA double strand breaks evidenced by a marked increase in the presence of γ-H2AX foci. This finding was also indicated by western blot, as well as cell cycle arrest by the phosphorylation of cyclin-dependent kinase 1. These data suggest that the three particle-types induce different degrees of DNA damage. And, of the three particle-types tested, exposure to ZnO nanoparticles may cause the most significant DNA damage.

Consuming Selected Groups of Products Among Polish and Spanish Physical Education Students Within the Context of the Assumptions Proposed by the Mediterranean Diet

2020 ◽  
Vol 30 (92) ◽  
pp. 15-16
Author(s):  
Maria Gacek ◽  
Grażyna Kosiba ◽  
Agnieszka Wojtowicz ◽  
Jacek Szalewski
Keyword(s):  
Physical Education ◽  
Mediterranean Diet ◽  
Statistical Significance ◽  
Red Meat ◽  
Poultry Meat ◽  
Processed Meat ◽  
Education Students ◽  
Physical Education Students ◽  
Frequent Consumption ◽  
The Mediterranean

Introduction: Nutritional behaviour is determined by individual and environmental factors. Aim: The aim of the study was to analyse the frequency of consuming selected groups of food products within the context of the recommendations proposed by the Mediterranean diet model, depending on the country of residence: Polish vs. Spanish physical education students. Material and methods: Research was carried out among 219 Polish and 280 Spanish students, using the standardised Kom-PAN questionnaire. In the statistical analysis, the chi-square test was used, at the α=0.05 level of statistical significance. Results: Nutritional mistakes of the general population were related to the low frequency of consuming: fruit, vegetables, wholemeal bread and other whole grains, fermented dairy products and vegetable oils, and the relatively frequent consumption of red meat, processed meat products and confectionery. Among the Polish students, significantly more frequent consumption of some products recommended in the Mediterranean diet (fruit, vegetables and wholegrain cereal products) as well as poultry meat was noted, but also more frequent consumption of sweets and confectionery products (p<0.001). The Spanish students significantly more often consumed the recommended dishes with legume seeds and sea fish (p<0.001), but also non-recommended products - red meat and fast food (p<0.01). Conclusions: Among Polish and Spanish physical education students, the assumptions of the Mediterranean diet were implemented to a limit extent, while depending on the country of residence, their differentiation was demonstrated.

scholarly journals Evaluation of the Protective Effects of Quercetin, Rutin, Naringenin, Resveratrol and Trolox Against Idarubicin-Induced DNA Damage

2010 ◽  
Vol 13 (2) ◽  
pp. 231 ◽  
Author(s):  
Haydar Çelik ◽  
Emel Arinç
Keyword(s):  
Dna Damage ◽  
Cytochrome P450 ◽  
Mitomycin C ◽  
Dna Strand Breaks ◽  
Protective Effects ◽  
Cytochrome P450 Reductase ◽  
Strand Breaks ◽  
P450 Reductase ◽  
Nadph Cytochrome P450 Reductase ◽  
Dna Strand

PURPOSE. Idarubicin is a synthetic anthracycline anticancer drug widely used in the treatment of some hematological malignancies. The studies in our laboratory have clearly demonstrated that idarubicin can undergo reductive bioactivation by NADPH-cytochrome P450 reductase to free radicals with resulting formation of DNA strand breaks, which can potentially contribute to its genotoxic effects [Çelik, H., Arinç, E., Bioreduction of idarubicin and formation of ROS responsible for DNA cleavage by NADPH-cytochrome P450 reductase and its potential role in the antitumor effect. J Pharm Pharm Sci, 11(4):68-82, 2008]. In the current study, our aim was to investigate the possible protective effects of several phenolic antioxidants, quercetin, rutin, naringenin, resveratrol and trolox, against the DNA-damaging effect of idarubicin originating from its P450 reductase-catalyzed bioactivation. METHODS. DNA damage was measured by detecting single-strand breaks in plasmid pBR322 DNA using a cell-free agarose gel method. RESULTS. Our results indicated that, among the compounds tested, quercetin was the most potent antioxidant in preventing DNA damage. Quercetin significantly decreased the extent of DNA strand breaks in a dose-dependent manner; 100 μM of quercetin almost completely inhibited the DNA strand breakage. Unlike quercetin, its glycosidated conjugate rutin, failed to provide any significant protection against idarubicin-induced DNA strand breaks except at the highest concentration tested (2 mM). The protective effects of other antioxidants were significantly less than that of quercetin even at high concentrations. Quercetin was found to be also an effective protector against DNA damage induced by mitomycin C. CONCLUSION. We conclude that quercetin, one of the most abundant flavonoids in the human diet, is highly effective in reducing the DNA damage caused by the antitumor agents, idarubicin and mitomycin C, following bioactivation by P450 reductase.

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