scholarly journals Beef meat promotion of dimethylhydrazine-induced colorectal carcinogenesis biomarkers is suppressed by dietary calcium

2008 ◽  
Vol 99 (5) ◽  
pp. 1000-1006 ◽  
Author(s):  
Fabrice Pierre ◽  
Raphaëlle Santarelli ◽  
Sylviane Taché ◽  
Françoise Guéraud ◽  
Denis E. Corpet
Keyword(s):  
Colorectal Cancer ◽  
Olive Oil ◽  
Control Diet ◽  
Red Meat ◽  
Aberrant Crypt Foci ◽  
Colorectal Carcinogenesis ◽  
Beef Meat ◽  
Antioxidant Agents ◽  
Increased Risk ◽  
High Calcium

Red meat consumption is associated with increased risk of colorectal cancer. We have previously shown that haemin, Hb and red meat promote carcinogen-induced preneoplastic lesions: aberrant crypt foci (ACF) and mucin-depleted foci (MDF) in rats. We have also shown that dietary Ca, antioxidant mix and olive oil inhibit haemin-induced ACF promotion, and normalize faecal lipoperoxides and cytotoxicity. Here we tested if these strategies are effective also against red meat promotion in dimethylhydrazine-induced rats. Three diets with 60 % beef meat were supplemented with calcium phosphate (31 g/kg), antioxidant agents (rutin and butylated hydroxyanisole, 0·05 % each) and olive oil (5 %). ACF, MDF, faecal water cytotoxicity, thiobarbituric acid reactive substances (TBARS) and urinary 1,4-dihydroxynonane mercapturic acid (DHN-MA) were measured. Beef meat diet increased the number of ACF (+30 %) and MDF (+100 %) (P < 0·001), which confirms our previous findings. Promotion was associated with increased faecal water TBARs ( × 4) and cytotoxicity ( × 2), and urinary DHN-MA excretion ( × 15). Ca fully inhibited beef meat-induced ACF and MDF promotion, and normalized faecal TBARS and cytotoxicity, but did not reduce urinary DHN-MA. Unexpectedly, high-calcium control diet-fed rats had more MDF and ACF in the colon than low-Ca control diet-fed rats. Antioxidant mix and olive oil did not normalize beef meat promotion nor biochemical factors. The results confirm that haem causes promotion of colon carcinogenesis by red meat. They suggest that Ca can reduce colorectal cancer risk in meat-eaters. The results support the concept that toxicity associated with the excess of a useful nutrient may be prevented by another nutrient.

scholarly journals Calcium carbonate suppresses haem toxicity markers without calcium phosphate side effects on colon carcinogenesis

2010 ◽  
Vol 105 (3) ◽  
pp. 384-392 ◽  
Author(s):  
Ossama Allam ◽  
Diane Bahuaud ◽  
Sylviane Taché ◽  
Nathalie Naud ◽  
Denis E. Corpet ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Calcium Carbonate ◽  
Calcium Phosphate ◽  
Metal Ion ◽  
Control Diet ◽  
Red Meat ◽  
Preneoplastic Lesions ◽  
Increased Risk ◽  
High Calcium

Red meat intake is associated with an increased risk of colorectal cancer. We have previously shown that haemin, Hb and red meat promote carcinogen-induced preneoplastic lesions, aberrant crypt foci (ACF), in the colon of rats. We have also shown that dietary calcium phosphate inhibits haemin-induced promotion and normalises faecal lipoperoxides and cytotoxicity. Unexpectedly, high-calcium phosphate control diet-fed rats had more preneoplastic lesions in the colon than low-Ca control diet-fed rats. The present study was designed to find a Ca supplementation with no adverse effect, by testing several doses and types of Ca salts. Onein vitrostudy and two short-term studies in rats identified calcium carbonate as the most effective Ca salt to bind haemin vitroand to decrease faecal biomarkers previously associated with increased carcinogenesis: faecal water cytotoxicity and thiobarbituric acid-reactive substances. A long-term carcinogenesis study in dimethylhydrazine-injected rats demonstrated that a diet containing 100 μmol/g calcium carbonate did not promote ACF, in contrast with a previously tested calcium phosphate diet. The results suggest that calcium carbonate, and not calcium phosphate, should be used to reduce haem-associated colorectal cancer risk in meat eaters. They support the concept that the nature of the associated anion to a protective metal ion is important for chemoprevention.

scholarly journals Impact of polymorphisms in DNA repair genes XPD, hOGG1 and XRCC4 on colorectal cancer risk in a Chinese Han Population

2019 ◽  
Vol 39 (1) ◽  
Author(s):  
Dexi Jin ◽  
Min Zhang ◽  
Hongjun Hua
Keyword(s):  
Colorectal Cancer ◽  
Gene Polymorphisms ◽  
Colorectal Carcinogenesis ◽  
Chinese Han Population ◽  
Control Group ◽  
Chinese Han ◽  
Han Population ◽  
Increased Risk ◽  
Hogg1 Gene ◽  
Repair Genes

Abstract Background: This research aimed to study the associations between XPD (G751A, rs13181), hOGG1 (C326G, rs1052133) and XRCC4 (G1394T, rs6869366) gene polymorphisms and the risk of colorectal cancer (CRC) in a Chinese Han population. Method: A total of 225 Chinese Han patients with CRC were selected as the study group, and 200 healthy subjects were recruited as the control group. The polymorphisms of XPD G751A, hOGG1 C326G and XRCC4 G1394T loci were detected by the RFLP-PCR technique in the peripheral blood of all subjects. Results: Compared with individuals carrying the XPD751 GG allele, the A allele carriers (GA/AA) had a significantly increased risk of CRC (adjusted OR = 2.109, 95%CI = 1.352–3.287, P=0.003). Similarly, the G allele (CG/GG) of hOGG1 C326G locus conferred increased susceptibility to CRC (adjusted OR = 2.654, 95%CI = 1.915–3.685, P<0.001). In addition, the T allele carriers (GT/TT) of the XRCC4 G1394T locus have an increased risk of developing CRC (adjusted OR = 4.512, 95%CI = 2.785–7.402, P<0.001). The risk of CRC was significantly increased in individuals with both the XPD locus A allele and the hOGG1 locus G allele (adjusted OR = 1.543, 95%CI = 1.302–2.542, P=0.002). Furthermore, individuals with both the hOGG1 locus G allele and the XRCC4 locus T allele were predisposed to CRC development (adjusted OR = 3.854, 95%CI = 1.924–7.123, P<0.001). The risks of CRC in XPD gene A allele carriers (GA/AA) (adjusted OR = 1.570, 95%CI = 1.201–1.976, P=0.001), hOGG1 gene G allele carriers (CG/GG) (adjusted OR = 3.031, 95%CI = 2.184–4.225, P<0.001) and XRCC4 gene T allele carriers (GT/TT) (adjusted OR = 2.793, 95%CI = 2.235–3.222, P<0.001) were significantly higher in patients who smoked ≥16 packs/year. Conclusion: Our results suggest that XPD G751A, hOGG1 C326G and XRCC4 G1394T gene polymorphisms might play an important role in colorectal carcinogenesis and increase the risk of developing CRC in the Chinese Han population. The interaction between smoking and these gene polymorphisms would increase the risk of CRC.

Antioxidant Agents and Colorectal Carcinogenesis: Role of β-Carotene, Vitamin E and Vitamin C

1996 ◽  
Vol 82 (1) ◽  
pp. 6-11 ◽  
Author(s):  
Giuseppe Pappalardo ◽  
Antonio Guadalaxara ◽  
Giuseppe Maiani ◽  
Giovanni Illomei ◽  
Mauro Trifero ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Vitamin E ◽  
Vitamin C ◽  
Colonic Mucosa ◽  
Genetic Alterations ◽  
Colorectal Carcinogenesis ◽  
Normal Colonic Mucosa ◽  
Antioxidant Agents ◽  
Β Carotene

In consideration of findings reported in the literature and of our study, we examined the correlation between antioxidants (β-carotene, vitamin C, vitamin E) and colorectal carcinogenesis. Although diagnostic progress has been made in the last decades, no significant improvements in death rates have been achieved in the western world. Exogenous factors might be responsible for a complex alteration process of normal colonic mucosa into adenoma and carcinoma. Free radicals and reactive oxygen metabolites, due to increased production or to reduced inactivation, following a decrease in the antioxidant burden in the mucosa, might cause damage to DNA, thereby resulting in genetic alterations. This might represent the cause of the transformation process: normal mucosa→ adenoma→ carcinoma. In a prospective study, we observed a reduction of β-carotene levels in normal colonic mucosa in patients with polyps and colorectal cancer. We also showed that β-carotene supplementation raises levels of this micronutrient in the colonic mucosa of these patients. Findings from the literature and our trials show a significant decrease in the antioxidant capacity of colorectal mucosa in patients affected by colorectal cancer, although there is a significant interindividual variability. Such results suggest a possible chemopreventive role of antioxidant agents in colorectal cancer.

scholarly journals Dietary Red Meat Adversely Affects Disease Severity in a Pig Model of DSS-Induced Colitis Despite Reduction in Colonic Pro-Inflammatory Gene Expression

Nutrients ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1728
Author(s):  
Tina S. Nielsen ◽  
Marlene Fredborg ◽  
Peter K. Theil ◽  
Yuan Yue ◽  
Lærke V. Bruhn ◽  
...  
Keyword(s):  
Control Diet ◽  
Clinical Signs ◽  
Epidemiologic Studies ◽  
Red Meat ◽  
Mucosal Inflammation ◽  
Negative Effects ◽  
Increased Risk ◽  
Meat Diet ◽  
Inflammatory Bowel ◽  
Systemic Health

Diet plays a substantial role in the pathogenesis and management of ulcerative colitis (UC), and epidemiologic studies indicate an association between red meat intake and increased risk of UC development. Therefore, we evaluated the effect of a red meat diet on dextran sulfate sodium (DSS)-induced colitis in pigs. Weaned pigs (42 days old) were fed either a control diet or a diet substituted with 15% minced, cooked and dried beef from experimental day 0 to 14. From day 14 to 18, half of the pigs on each diet received a daily oral dose of DSS. Dietary red meat aggravated the severity of colitis based on clinical signs of disease (negative performance score) and histopathological parameters in the colon such as erosion/ulceration and the overall inflammation score but no negative effects were observed on systemic health or small intestinal permeability. Importantly, dietary meat also caused a potential beneficial reduction in the colonic expression of the pro-inflammatory cytokines IL-17A and IL-6, the pro-inflammatory enzyme PTGS2 and in the chemokine IL-8. The present study emphasizes the potential of diet to modulate mucosal inflammation and that a red meat diet might be a risk factor for the development of inflammatory bowel disease.

scholarly journals The High-Fat Diet Based on Extra-Virgin Olive Oil Causes Dysbiosis Linked to Colorectal Cancer Prevention

Nutrients ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1705
Author(s):  
Carmen Rodríguez-García ◽  
Cristina Sánchez-Quesada ◽  
Ignacio Algarra ◽  
José J. Gaforio
Keyword(s):  
Colorectal Cancer ◽  
Gut Microbiota ◽  
Olive Oil ◽  
High Fat Diet ◽  
Virgin Olive Oil ◽  
Extra Virgin Olive Oil ◽  
High Fat ◽  
Inflammatory Microenvironment ◽  
Increased Risk ◽  
Colorectal Cancer Prevention

The present study aims to examine the effects of three different high-fat diet (HFD) on mice gut microbiota in order to analyse whether they create the microenvironmental conditions that either promote or prevent colorectal cancer (CRC). We evaluated colonic mucosa-associated microbiota in CD1 mice fed with HFD, based on 60% kcal from fat-containing coconut, sunflower or extra-virgin olive oil as the only source of fat. The main findings were as follows: (a) All HFD produced a decrease in the richness and diversity of the intestinal microbiota that was independent of mouse weight, (b) HFD switched Lactobacillus to Lactococcus. In general, the results showed that both sunflower- and coconut-HFD generated a pro-inflammatory intestinal microenvironment. In brief, coconut-HFD decreased Akkermansia and increased Staphylococcus, Prevotella and Bacteroides spp. abundance. Sunflower-HFD reduced Akkermansia and Bifidobacterium, while enhancing Sphingomonas and Neisseria spp. abundance. In contrast, EVOO-HFD produced an anti-inflammatory microenvironment characterised by a decreased Enterococcus, Staphylococcus, Neisseria and Pseudomonas spp. abundance. At the same time, it increased the Firmicutes/Bacteroidetes ratio and maintained the Akkermansia population. To conclude, EVOO-HFD produced changes in the gut microbiota that are associated with the prevention of CRC, while coconut and sunflower-HFD caused changes associated with an increased risk of CRC.

scholarly journals Title: Risk Factors for the Diagnosis of Colorectal Cancer

2022 ◽  
Vol 29 ◽  
pp. 107327482110566
Author(s):  
Anna Lewandowska ◽  
Grzegorz Rudzki ◽  
Tomasz Lewandowski ◽  
Aleksandra Stryjkowska-Góra ◽  
Sławomir Rudzki
Keyword(s):  
Physical Activity ◽  
Colorectal Cancer ◽  
Risk Factors ◽  
Meat Consumption ◽  
Red Meat ◽  
World Health ◽  
Control Group ◽  
Group I ◽  
Increased Risk ◽  
Group Ii

Background Colorectal cancer defined as cancer of the colon or rectum, is the third most frequently diagnosed cancer in men and the second in women, and, according to the World Health Organization database GLOBOCAN, it accounts for nearly 1.4 million new cases annually worldwide. The occurrence of colorectal cancer is associated with nonmodifiable risk factors, including age and hereditary factors, as well as with modifiable environmental and lifestyle factors. Methods The study included 800 patients, 400 diagnosed with colorectal cancer and 400 within the control group, who gave their written informed consent to participate in the study. Patients with cancer other than colorectal cancer were randomly selected for control group I, and patients with no cancer diagnosis were selected for control group II. The method used was a case-control study – an observational and analytical study with a control group, conducted among patients of the Clinical Oncology Centre and the Provincial Hospital in the years 2019–2020. The study comparing the exposure was carried out in a group of people who developed the endpoint, that is colorectal cancer, with the exposure in a well-matched group of controls who did not reach the endpoint. Assessment of activity and BMI was used according to WHO recommendations, as well as the expert system. The data were tested for the distribution and the homogeneity of variance was validated before applying the parameter tests. Comparison of quantitative variables between groups was performed using ANOVA. Results The mean age of the patients was 64.53 ± 8.86 years, of the control group I – 59.64 ± 9.33 and the control group II – 57.5 (7.83). There was a strong positive association between the incidence of ulcerative colitis and the risk of colorectal cancer ( P < .01). Among obese subjects, the risk of developing colorectal cancer was 1.27 (95% CI, 1.06–1.53) compared with nonobese subjects. A strong positive relationship was found between low physical activity converted to metabolic equivalent of MET effort per week and the risk of colorectal cancer ( P < .001). The relative risk for current smokers was 2.17 (95% CI 1.79–2.66). There was an association between higher fat consumption and higher red meat consumption and the risk of developing colorectal cancer ( P < .01). Conclusions Obesity, low physical activity, active and passive smoking and high salt and red meat consumption have been associated with an increased risk of colorectal cancer. These findings provide further evidence of the importance of maintaining a healthy lifestyle.

scholarly journals Red Meat-Derived Nitroso Compounds, Lipid Peroxidation Products and Colorectal Cancer

Foods ◽  
2019 ◽  
Vol 8 (7) ◽  
pp. 252 ◽  
Author(s):  
Steinberg
Keyword(s):  
Colorectal Cancer ◽  
Lipid Peroxidation ◽  
Gastrointestinal Tract ◽  
Gene Mutations ◽  
Red Meat ◽  
Heme Iron ◽  
Dna Lesions ◽  
Colorectal Carcinogenesis ◽  
Nitroso Compounds ◽  
First Time

About 20 years ago, the research group of Sheila Anne Bingham in Cambridge, UK, showed for the first time that volunteers consuming large amounts of red meat excrete high amounts of nitroso compounds via feces. In the meantime, it has been demonstrated that heme leads to the enhanced formation of nitroso compounds in the gastrointestinal tract and that the main nitroso compounds formed in the gastrointestinal tract are S-nitrosothiols and the nitrosyl heme. Moreover, it has been postulated that these endogenously formed nitroso compounds may alkylate guanine at the O6-position, resulting in the formation of the promutagenic DNA lesions O6-methylguanine and O6-carboxymethylguanine, which, if not repaired (in time), could lead to gene mutations and, subsequently to the development of colorectal cancer. Alternatively, it has been postulated that heme iron could contribute to colorectal carcinogenesis by inducing lipid peroxidation. In the present review, the evidence supporting the above-mentioned hypotheses will be presented.

scholarly journals PLZF Expression during Colorectal Cancer Development and in Normal Colorectal Mucosa according to Body Size, as Marker of Colorectal Cancer Risk

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Francesco Mariani ◽  
Paola Sena ◽  
Giulia Magnani ◽  
Stefano Mancini ◽  
Carla Palumbo ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Risk ◽  
Colonic Mucosa ◽  
Zinc Finger Protein ◽  
Strong Association ◽  
Aberrant Crypt Foci ◽  
Colorectal Carcinogenesis ◽  
Normal Colonic Mucosa ◽  
Anthropometric Parameters ◽  
Colorectal Mucosa

Promyelocytic leukemia zinc finger protein (PLZF) is a protein involved in various signaling, growth regulatory, and differentiation pathways, including development/function of some T cells. Here, we aimed at the detection of PLZF during colorectal carcinogenesis, using immunofluorescence, and at the evaluation of the colocalization of PLZF with CD2 and CD56 positive cells (T,γδ, NK, and NKT cells), using confocal-microscopy, along colorectal carcinogenesis, since its earliest stages, that is, dysplastic aberrant crypt foci (ACF). Furthermore, we analyzed PLZF in the normal colonic mucosa (NM) according to anthropometric parameters of the subject. NM exhibited strong CD56 fluorescent staining. This infiltration was lost in both ACF and colorectal carcinoma (CRC), while PLZF presence increased from NM to ACF and CRC. Strong association was found between CD56+ colonic mucosa cell infiltration and body mass index. Interestingly, an increased stromal PLZF-reactivity was present in NM of obese subjects. This study shows that overexpression of PLZF and exclusion of NK cells in dysplastic microenvironment are very early events in the stepwise sequence leading to CRC and that lower levels of CD56+ cells in NM, together with increased levels of PLZF+ cells, can be a reflection of colon cancer risk due to obesity.

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