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A review of the literature reveals a very consistent association between gastric cancer risk and low intake of fruits and vegetables. This observation has been documented in many countries with different epidemiological techniques: interpopulation correlations, case-control studies and follow up of several cohorts. Low serum levels of beta-carotene and alpha-tocopherol, but not vitamin C, have been reported in patients with gastric dysplasia. Helicobacter pylori infection has been associated with lower concentrations of vitamin C in the gastric juice. Detailed studies in Colombia and New Orleans have shown a gradient towards lower concentration in the gastric juice and lower ratios of gastric juice to serum concentration of vitamin C in the following comparisons: i) lower vs. higher gastric cancer risk; ii) mild vs. advanced gastric precancerous histopathologic lesions; iii) mild vs. advanced degree of atrophy; iv) mild vs. advanced damage to the surface gastric epithelium; v) lower vs. higher gastric pH. Such a gradient is not observed for serum levels of vitamin C. The role of infection with H. pylori in the metabolism of ascorbic acid is discussed, as well as the possible role of ascorbic acid in inhibiting cell damage by reactive oxygen species.
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PMID:Review article: Antioxidant micronutrients and gastric cancer. 970 Oct 5

Helicobacter pylori infection in humans is associated with chronic type B gastritis, peptic ulcer disease, and gastric carcinoma. A high intake of carotenoids and vitamin C has been proposed to prevent development of gastric malignancies. The aim of this study was to explore if the microalga Haematococcus pluvialis rich in the carotenoid astaxanthin and vitamin C can inhibit experimental H. pylori infection in a BALB/cA mouse model. Six-week-old BALB/cA mice were infected with the mouse-passaged H. pylori strain 119/95. At 2 weeks postinoculation mice were treated orally once daily for 10 days (i) with different doses of algal meal rich in astaxanthin (0.4, 2, and 4 g/kg of body weight, with the astaxanthin content at 10, 50, and 100 mg/kg, respectively), (ii) with a control meal (algal meal without astaxanthin, 4 g/kg), or (iii) with vitamin C (400 mg/kg). Five mice from each group were sacrificed 1 day after the cessation of treatment, and the other five animals were sacrificed 10 days after the cessation of treatment. Culture of H. pylori and determination of the inflammation score of the gastric mucosae were used to determine the outcome of the treatment. Mice treated with astaxanthin-rich algal meal or vitamin C showed significantly lower colonization levels and lower inflammation scores than those of untreated or control-meal-treated animals at 1 day and 10 days after the cessation of treatment. Lipid peroxidation was significantly decreased in mice treated with the astaxanthin-rich algal meal and vitamin C compared with that of animals not treated or treated with the control meal. Both astaxanthin-rich algal meal and vitamin C showed an inhibitory effect on H. pylori growth in vitro. In conclusion, antioxidants may be a new strategy for treating H. pylori infection in humans.
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PMID:Astaxanthin-rich algal meal and vitamin C inhibit Helicobacter pylori infection in BALB/cA mice. 1095 94

Low gastric juice total vitamin C concentration in the presence of Helicobacter pylori infection probably plays a role in gastric carcinogenesis. Vitamin C plays a role in the neutralization of various pathogenic factors connected with H. pylori infection, including the destruction of free radicals, which damage tissues and cell DNA, and inhibition of the formation of N-nitroso compounds, which have a strong carcinogenic activity. The aim of the study was to determine whether tobacco smoking had any effect on gastric juice vitamin C concentration in healthy subjects and in patients infected with H. pylori. Eighty-six patients with dyspeptic symptoms undergoing routine endoscopy entered the study after giving informed consent. In all patients plasma and gastric juice total vitamin C levels were measured by a spectrophotometric method. They were entered into four groups: group I (controls) - H. pylori-negative non-smokers (n = 17), group II - H. pylori-negative smokers (n = 16), group III - non-smokers with H. pylori infection (n = 21), and group IV - H. pylori-infected smokers (n = 32). In the control group (I) the mean gastric juice total vitamin C concentration was 17.1 microg/ml (range 5.3-40.0 microg/ml), which was significantly higher (P < 0.05) than in group II (12.6 microg/ml, range 5.1-21.0 microg/ml), group III (5.8 microg/ml range 2.1-13.7 microg/ml) and group IV (3.9 microg/ml, range 1.1-10.6 microg/ml) (P < 0.001). Statistically significant differences also were noted between groups II and III (P < 0.01) and groups II and IV (P < 0.001) and between groups III and IV (P < 0.05). These results demonstrate that the concentration of vitamin C in gastric juice is significantly lower in smokers than in non-smokers. This was observed in healthy subjects as well as H. pylori-infected patients. This phenomenon may be one of the mechanisms whereby smoking contributes to the production of gastric lesions, impairs healing of peptic ulcers and also increases the recurrence rate of peptic ulcers in cases with H. pylori infection.
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PMID:Tobacco smoking and vitamin C concentration in gastric juice in healthy subjects and patients with Helicobacter pylori infection. 1120 81

Patients infected with Helicobacter pylori have abnormally low ascorbic acid concentration in gastric juice. Low vitamin C intake and Helicobacter pylori infection have been related to an increased risk of gastric carcinoma. This report examines the association between ascorbic acid and Helicobacter pylori in patients referred for upper gastrointestinal endoscopy. Elevated gastric pH and the damage to the gastric surface epithelium were inversely associated with the ascorbic acid concentration in gastric juice. We postulate that these two factors mediate the ascorbic acid-decreasing effect of Helicobacter pylori. Patients with nonpremalignant conditions (normal gastric histology, diffuse antral gastritis, or duodenal ulcer) had lower gastric pH, less damage to the gastric epithelium, and higher levels of ascorbic acid in gastric juice than patients with atrophic gastritis, intestinal metaplasia, or dysplasia.
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PMID:Helicobacter pylori-associated gastritis and the ascorbic acid concentration in gastric juice. 1130 11

Helicobacter pylori infection is associated with elevated gastric mucosal concentrations of the lipid peroxidation product malondialdehyde and reduced gastric juice vitamin C concentrations. Malondialdehyde can react with DNA bases to form the mutagenic adduct malondialdehyde-deoxyguanosine (M(1)-dG). We aimed to determine gastric mucosal levels of M(1)-dG in relation to H. pylori infection and malondialdehyde and vitamin C concentrations. Patients (n = 124) attending for endoscopy were studied. Levels of antral mucosal M(1)-dG were determined using a sensitive immunoslot-blot technique; antral mucosal malondialdehyde was determined by thiobarbituric acid extraction, and gastric juice and antral mucosal ascorbic acid and total vitamin C were determined by high-performance liquid chromatography. Sixty-four H. pylori-positive patients received eradication therapy, and endoscopy was repeated at 6 and 12 months. Levels of M(1)-dG did not differ between subjects with H. pylori gastritis (n = 85) and those with normal mucosa without H. pylori infection (n = 39; 56.6 versus 60.1 adducts/10(8) bases) and were unaffected by age or smoking habits. Malondialdehyde levels were higher (123.7 versus 82.5 pmol/g; P < 0.001), gastric juice ascorbic acid was lower (5.7 versus 15.0 micromol/ml; P < 0.001), and antral mucosal ascorbic acid was unchanged (48.0 versus 42.7 micromol/g) in H. pylori gastritis compared with normal mucosa. Multiple regression analysis revealed that M(1)-dG increased significantly with increasing levels of malondialdehyde, antral ascorbic acid, and total antral vitamin C. M(1)-dG levels were unchanged 6 months (63.3 versus 87.0 adducts/10(8) bases; P = 0.24; n = 38) and 12 months (66.7 versus 77.5 adducts/10(8) bases; P = 0.8; n = 13) after successful eradication of H. pylori. M(1)-dG thus is detectable in gastric mucosa, but is not affected directly by H. pylori.
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PMID:Levels of malondialdehyde-deoxyguanosine in the gastric mucosa: relationship with lipid peroxidation, ascorbic acid, and Helicobacter pylori. 1131 78

The results of recent investigations have suggested that the old hypothesis of an atrophy-metaplasia-dysplasia-carcinoma sequence in the stomach needs to be qualified. The most common cause of intestinal metaplasia is Helicobacter pylori gastritis. The consequence of this intestinal metaplasia is focal atrophy. Helicobacter pylori infection may also trigger an autoimmune gastritis of the corpus mucosa, with atrophy and intestinal metaplasia. Most intestinal metaplasias are only 'paracancerous' but not 'precancerous' lesions. Diffuse gastric carcinomas, such as the signet ring cell carcinoma, arise independently of intestinal metaplasia. Histogenetically, numerous carcinomas of the stomach are primarily of the gastric type, and may secondarily change into the intestinal type.High-grade intra-epithelial neoplasias (dysplasias) detected during the biopsy-based diagnostic work-up appear to be a marker for carcinoma and must, therefore, be removed endoscopically. The detection of intestinal metaplasia in routinely obtained biopsy material is subject to sampling error and is, therefore, not a suitable marker for an increased risk of a gastric carcinoma developing. As an alternative, the concept of gastritis of the carcinoma phenotype, which is more frequently found in early gastric carcinomas and in the relatives of gastric carcinoma patients, has been developed. In this concept, the diffuse parameters of grade and activity of the gastritis in the antrum and corpus, which are independent of sampling error, are subjected to a comparative analysis. A risk gastritis of the carcinoma phenotype is diagnosed when the grade and activity of the gastritis in the corpus are at least equally as pronounced as in the antrum. Currently, this concept is being tested in a prospective ongoing study. Future studies must show whether, and if so which, immunohistochemical or molecular-genetically detectable changes can be applied as risk markers in the diagnostic work-up. Helicobacter pylori eradication probably does not lead to complete regression of the intestinal metaplasia and ensuing focal atrophy. However, eradication of H. pylori does lead to the normalization of changes that can lead to mutations of the stem cells of the gastric mucosa (free radicals, nitric oxide, cell proliferation and vitamin C secretion).
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PMID:Atrophy-metaplasia-dysplasia-carcinoma sequence in the stomach: a reality or merely an hypothesis? 1186 88

Antioxidants are substances capable of inhibiting oxidation. In chronic diseases, inflammatory response cells produce oxygen free radicals. Oxygen free radicals cause DNA damage, and this may lead to gene modifications that might be carcinogenic. Chronic Helicobacter pylori infection causes the production of DNA-damaging free radicals. In recent years, various groups have studied the effects of antioxidants, especially on H. pylori-associated gastric cancer. In most of the studies, it has been shown that H. pylori infection does affect the level of antioxidants measured in the gastric juice, but there are also controversial results. Recent experimental studies, both in vivo and in vitro, have shown that vitamin C and astaxanthin, a carotenoid, are not only free radical scavengers but also show antimicrobial activity against H. pylori. It has been shown that astaxanthin changes the immune response to H. pylori by shifting the Th1 response towards a Th2 T-cell response. Very few experimental studies support the epidemiologic studies, and further studies are needed to describe the effect and the mechanism of antioxidants in the H. pylori immune response.
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PMID:Effect of antioxidants on the immune response of Helicobacter pylori. 1219 57

There is great evidence that both gastric lymphoma andadenocarcinoma are related in their pathogenesis to Helicobacter pylori infection.It has been stablished that mucosa associated lymphoid tissue (MALT) is anacquired condition following H. pylorl infection and that B cell gastriclymphoma derives from this cell linage. Low grade MALT lymphoma transformsto high grade lymphoma. Furthermore, MALT B cell lymphoma seems toproliferate in response to an antigenic stimulus provided by T cell line of cells specificately activated by H. pylori. The use of antibiotics in the erradication of H. pylori is considered one of the strongest evidence for this association, based on the remission rates of gastric MALT lymphoma.For adenocarcinoma the rationale is: H. pylori induces chronic superficialgastritis and profound gastritis; the effect of the bacteria itself,nutritional and inmunological factors as well as the asumption of funtionalhyposecretion, could lead to an atrophic phenomena, intestinal metaplasia, dysplasia and finally adenocarcinoma. An hypoclorhidric/aclorhidric condition produced due to atrophy of the mucosa and a relative funtional state, lead to bacterial overgrowth with the subsequente production of N-nitrous compounds, well known because of its mutagenic and carcinogenic effects.Also, the secretion of vitamin C and ascorbic acid which have a protective mechamism against free radicals and decreasing production of N-nitrous compound formation, are afected for H. pylori infection.
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PMID:[THE ROL OF HELICOBACTER PYLORI IN GASTRODUODENALTUMOROUS PATHOLOGY] 1229 74

Established risk factors for gastric cancer include a diet high in nitrate or nitrite and low in vitamin C and the presence of achlorhydria or hypochlorhydria. The aim of this study was to investigate the relationship between intragastric nitrite concentration and atrophic change of the stomach or gastric carcinogenesis in Japanese Helicobacter pylori-infected patients. Gastric juice pH, nitrite, and total vitamin C concentrations in gastric juice, serum pepsinogen I and II concentrations, and specific Helicobacter pylori antibody were analyzed. Intragastric total vitamin C concentration was decreased by Helicobacter pylori infection of the gastric mucosa and with progression of the atrophic grade. There was a significant positive correlation between atrophic grade and intragastric nitrite concentration. In conclusion, the levels of nitrite in gastric juice play a causal role in the development of cancer in Helicobacter pylori-associated atrophic gastric mucosa.
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PMID:Does intragastric nitrite concentration reflect gastric carcinogenesis in Japanese Helicobacter pylori-infected patients? 1456 Sep 92

A hospital-based case-control study of 295 cases with histologically confirmed gastric cancer and age and sex-matched controls was conducted to evaluate the effect of dietary vitamin C intake upon the relation between Helicobacter pylori infection and gastric cancer in Korea in 1997-1998. Anti-H. pylori IgG was detected by ELISA. A food frequency questionnaire, and a questionnaire on demographic factors, including past medical history, smoking, alcohol consumption, and life style was also administered. The prevalences of H. pylori IgG in cases and controls were 80.7% and 71.2%, respectively, and the odds ratio (OR) of H. pylori for gastric cancer was 1.68 (95% confidence interval (CI): 1.14, 2.44), after adjusting for age, sex, educational level, and a past medical history of gastritis or gastric ulcer. In a stratified analysis, H. pylori seropositivity was found to be a significant risk factor for gastric cancer in the low vitamin C intake group (OR = 4.68; 95% CI: 1.97, 11.1), but not in the high vitamin C intake group (OR = 0.72; 95% CI: 0.32, 1.65). Vitamin C intake was found to modify the relation between H. pylori and gastric cancer.
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PMID:Effect modification by vitamin C on the relation between gastric cancer and Helicobacter pylori. 1575 6


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