Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: DrugBank:EXPT00568 (ascorbate)
 23,072 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Risks for gastric cancer in relation to diet and other environmental factors are receiving renewed attention. New developments include the emerging relationship between Helicobacter pylori infection and an increased risk for gastric cancer, and positive results of chemoprevention trials in decreasing gastric cancer risk with the use of beta-carotene and vitamin E supplements. Factors that may enhance risk include consumption of nitrites, nitrates, alcohol, and highly salted, pickled, fermented, or smoked foods. Other environmental factors which may promote cancer are H. pylori infection, inappropriate food storage, metal and cement dust exposure, and cigarette smoking. High intakes of fruits and vegetables or of antioxidants, such as beta-carotene, vitamin E, and vitamin C may decrease risk.
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PMID:Diet, Helicobacter pylori infection, food preservation and gastric cancer risk: are there new roles for preventative factors? 801 50

Gastric juice ascorbic acid concentrations were examined in black and white patients. Significantly lower concentrations were found in blacks, in the absence of a significant difference in the plasma concentration of vitamin C between races. Blacks had higher prevalence of Helicobacter pylori infection, higher gastric pH, more severe acute and chronic inflammation of the gastric mucosa and higher frequency of Lewis (a-b-) phenotype. Although most of these factors have been related to low ascorbic acid levels in gastric juice, none of them could account entirely for the difference between races either individually or after joint consideration. These observations may help to explain the high incidence of gastric carcinoma among the black population in southern Louisiana.
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PMID:Ascorbic acid, Helicobacter pylori and Lewis phenotype among blacks and whites in New Orleans. 808 May 90

The incidence of gastric cancer varies widely by country and population, with higher rates among the lower socioeconomic groups. Although the most common cause of cancer death in the United States in 1930, its incidence has decreased dramatically during the past 60 years. Most populations show a 2-1 ratio for male to female gastric cancer cases, and a higher incidence rate among United States blacks than whites. Although rates have generally decreased, there has been a dramatic increase in the incidence of gastric cancer in the cardia. Diet has been the most studied risk factor for gastric cancer. Of particular interest have been N-nitroso compounds derived from the consumption of preserved, smoked, and cured foods. An inverse association with the consumption of fruits and vegetables has also been consistently demonstrated, though the specific nutrient(s) that this represents has been unclear, although ascorbate and beta-carotene have been intensively studied. Among nondietary factors, substantial evidence has accumulated for an increased risk with Helicobacter pylori infection. Other exposures which have been fairly consistently associated with gastric cancer include cigarette smoking, partial gastrectomy, radiation exposure, family history, pernicious anemia, blood group A, certain occupational exposures, and Epstein-Barr virus.
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PMID:Epidemiology of gastric cancer. 865 12

We have evaluated gastric juice pH, nitrites and vitamin C levels, mucosal glutathione, and malondialdehyde, a marker of lipid peroxidation, in patients with chronic gastritis undergoing endoscopy. Patients had chronic gastritis with (n = 28) or without (n = 60) atrophy and/or concomitant Helicobacter pylori infection. Nineteen healthy subjects, without major macroscopic or histologic changes, were included as controls. Ten subjects were studied before and after H. pylori eradication. Vitamin C levels were low in atrophic gastritis (p < 0.006) and H. pylori infection (p < 0.02). Nitrite concentrations and pH were significantly higher in atrophy (p < 0.005 and 0.0001). Glutathione turnover was higher than normal in gastritis, with higher levels of oxidized glutathione (p < 0.02). Gastric malondialdehyde levels were significantly increased by gastritis (p < 0.05) and H. pylori infection (p < 0.05). Overall, more active gastritis coincided with lower vitamin C levels and higher malondialdehyde levels. After H. pylori eradication a drop in mucosal MDA levels was observed (p = 0.04). In summary, chronic gastritis and H. pylori infection correlate with increased free-radical production, reduced gastric vitamin C levels, and increased glutathione turnover. The possible implications of these changes in the pathogenesis of gastric damage and in carcinogenesis are intriguing.
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PMID:Gastric antioxidant, nitrites, and mucosal lipoperoxidation in chronic gastritis and Helicobacter pylori infection. 877 22

A double-blind, placebo-controlled trial is being conducted in a population at high risk for gastric cancer in Venezuela. The main aim of the trial is to assess the effect of antioxidant vitamins (beta-carotene, vitamin C and vitamin E) in blocking the progression of precancerous lesions of the stomach. Within the framework of a screening programme for stomach cancer, 2200 subjects of 35-69 years of age have been recruited. At study entry, a dietary questionnaire was completed, and gastroscopy with the collection of seven gastric biopsies was performed. After baseline examinations, the study participants were randomized to receive antioxidant treatment or placebo for three years. The treatment phase will be completed in mid-1998. At the end of the treatment phase, the investigations performed at study entry will be repeated. Before the initiation of the trial, various pilot studies were carried out that showed an extremely high prevalence of Helicobacter pylori infection (over 90%). Two eradication trials using anti-H. pylori treatments that give good results in Europe and North America gave very poor results in our study population. The low eradication rates achieved (5-20%) suggest a high prevalence of antibiotic-resistant H. pylori strains or high reinfection rates. These disappointing results led to deletion of an anti-H. pylori treatment phase of the main trial.
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PMID:Chemoprevention trial on precancerous lesions of the stomach in Venezuela: summary of study design and baseline data. 892 24

In many Western developed countries, the incidence of stomach cancer has declined dramatically. This decrease was an extraordinary, "unplanned triumph", especially when compared to other cancers. Stomach cancer is still the most prevalent malignant tumor in Korea. Most Koreans carry Helicobacter pylori in their stomach. Thus, a new hypothesis, based on the relationship between the host and Helicobacter pylori, is presented as the carcinogenesis of human stomach cancer. The reasons for why the N-nitrosamide hypothesis should be dismissed as the etiology of stomach cancer, and why the contemporarily available principles and practice of intervention strategies to rapidly decrease the surprisingly high prevalence rate of Helicobacter pylori infection are impractical at this moment, are explained. In order to introduce an alternative provisional strategy of the "planned triumph" for the population vulnerable to stomach cancer, vitamin C is defined as an anti-inflammatory agent on the basis of the pathogenesis of Helicobacter pylori infection.
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PMID:Pathogenesis and prevention of stomach cancer. 893 91

Stomach cancer remains a common type of cancer, though its incidence has been halved in the last forty years. It is unevenly distributed throughout the world. In France, it holds fifth place among cancers and there are 8700 new cases each year. Helicobacter pylori infection, a high salt intake as well as an inadequate diet take part in the first stages of carcinogenesis. Later on, nitrates and nitrites, polycyclic hydrocarbons, alcohol, tobacco and bilc acids are incriminated. The protective role of vegetables and fruit has been well established. The protective role of vitamin C and beta-carotene is currently undergoing evaluation in subjects suffering from precancerous conditions such as dysplasia and incomplete intestinal metaplasia. The development of a vaccine against Helicobacter pylori induced infection also represents an important goal.
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PMID:[Epidemiology and etiology of malignant gastric tumors]. 918 59

Several lines of evidence support an association between Helicobacter pylori infection and gastric cancer. The natural history of H. pylori-associated gastritis is inexorable progression ultimately leading to gastric atrophy. In general, this process requires between 20 and 40 years to complete. Atrophic gastritis is widely considered to be a precursor lesion of the intestinal type of gastric cancer. Moreover, areas with a high prevalence of H. pylori infection also have a high prevalence of gastric cancer. Strong evidence from three prospective studies shows the risk of gastric cancer to be increased fourfold in H. pylori-positive persons. Several retrospective studies have also confirmed that H. pylori infection is associated with development of gastric cancer, especially in the younger generation, early gastric cancer, and noncardiac gastric cancer. H. pylori alone is not likely responsible for gastric cancer. Rather, it may provide a suitable environment, including chronic gastritis and intestinal metaplasia, for neoplastic change. Recognition of an association between H. pylori infection and gastric cancer has led to a major shift in emphasis on the cause of the disease. Research into H. pylori has focused attention on the importance of chronic inflammation and impaired host defense mechanisms as factors in the development of gastric cancer. H. pylori infection leads to changes in many factors that are important to the pathogenesis of gastric cancer, including vitamin C content of gastric juice, reactive oxygen metabolites, and epithelial cell proliferation. Eradication of the organism may reverse these changes. Therefore, eradication of H. pylori in infected persons might be a route to preventing gastric cancer, although many questions still remain as to the effectiveness of this strategy.
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PMID:What role does Helicobacter pylori play in gastric cancer? 939 61

Based on the findings of several epidemiological studies, it is believed that Helicobacter pylori infection is closely associated with gastric cancer. Because some abnormalities, such as severe inflammation in the gastric mucosa, impaired secretion of vitamin C, and increased gastric cell proliferation, improve after cure of the infection, anti-H. pylori therapy may reduce the incidence of gastric cancer. In Japan, the odds ratios for the development of atrophic gastritis and gastric cancer in H. pylori-positive patients are not as high as those reported in Europe and the United States. These findings suggest that factors other than H. pylori may exert a considerable influence on the development of atrophic gastritis and gastric cancer in Japan. It is not known whether atrophy and intestinal metaplasia, possible precursors of gastric cancer, are reversible. H. pylori infection is associated with a "gastritis, intestinal metaplasia, and gastric cancer sequence," but it remains obscure whether the infection is directly associated with the development of gastric cancer. We do not know which age group of patients should be given anti-H. pylori therapy for the prevention of gastric cancer. To elucidate whether the eradication of H. pylori can prevent gastric cancer, a Japanese intervention trial is now in progress.
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PMID:What remaining questions regarding Helicobacter pylori and associated diseases should be addressed by future research? View from the Far East. 939 78

Low intake of foods rich in vitamin C is associated with an increased risk of gastric cancer, and geographic variation in average vitamin C intake, therefore, could explain some of the wide international variation in gastric cancer rates. This multicentre study investigated the relationships between plasma levels of vitamin C, as an indicator of vitamin C intake, and gastric cancer rates, markers of gastritis and other socio-demographic variables. Fasting plasma samples from about 1,400 individuals from 9 centres in 7 countries worldwide were assayed for total vitamin C using a fluorometric assay. There was no association between average plasma vitamin C levels and either gastric cancer mortality or incidence rates in the populations studied. Therefore, variation in fasting plasma vitamin C levels, as an indicator of consumption of vitamin C, does not appear to explain any of the wide geographic variation in gastric cancer rates. Furthermore, there was no association between plasma vitamin C levels and Helicobacter pylori infection, low serum levels of pepsinogen A (as a marker of severe chronic atrophic gastritis) or the presence of DNA adducts in blood leukocyte DNA. Multivariate models showed that fasting plasma vitamin C levels were associated positively with female sex, higher levels of education, never having smoked and increasing height and negatively with number of cigarettes smoked per day and increasing weight. This suggests not only that gender and tobacco smoking, in particular, are important predictors of plasma vitamin C levels but also that their effects are consistent throughout the developed world.
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PMID:Gastric cancer, gastritis and plasma vitamin C: results from an international correlation and cross-sectional study. The Eurogast Study Group. 939 46


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