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This study argues that H.pylori infection, by increasing the production of reactive oxygen species, increases the utilization of dietary antioxidants(Vit E and Vit C) that serve in quenching the free radicals, thus decreasing their serum levels and confounding their protective effect against gastric cancer.
It has been postulated that dietary antioxidants may reduce cancer risk by modulating red-ox status, by preventing biological oxidation, and by inhibiting the formation of carcinogen. However, supplementation studies and prospective studies have yielded contradictory results. In the case of gastric cancer, H.pylori infection, which is known to be associated with a higher risk of the disease, results in an increased production of ROS & RNS. As a result serum levels of these free radicals increase, exerting a higher demand for dietary antioxidants to neutralize them.
The fact that the relation between serum levels of antioxidants and gastric cancer is more consistent than that of dietary intake levels and the disease suggests the possibility of the presence of an intrinsic factor that is altering the true relation between dietary antioxidants and the cancer. This intrinsic factor, this study argues, is the infection with H.pylori.
H.pylori infection, by increasing the production of reactive oxygen species, increases the utilization of dietary antioxidants that serve in quenching the free radicals, thus decreasing their serum levels and confounding their protective effect against gastric cancer. The purpose of this pilot study is to investigate the possibility that H.pylori infection alters the bioavailability of the dietary antioxidants: vitamin C, and vitamin E. This project will be done in preparation for an etiologic study of dietary antioxidants and gastric cancer.
Allocation: Non-Randomized, Control: Active Control, Endpoint Classification: Pharmacokinetics/Dynamics Study, Intervention Model: Parallel Assignment, Masking: Open Label, Primary Purpose: Prevention
Heliobacter Pylori Infection
vitamin C & E supplements
Toronto General Hospital
Active, not recruiting
University of Toronto
Published on BioPortfolio: 2014-08-27T03:45:42-0400
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A nutritional condition produced by a deficiency of VITAMIN B 12 in the diet, characterized by megaloblastic anemia. Since vitamin B 12 is not present in plants, humans have obtained their supply from animal products, from multivitamin supplements in the form of pills, and as additives to food preparations. A wide variety of neuropsychiatric abnormalities is also seen in vitamin B 12 deficiency and appears to be due to an undefined defect involving myelin synthesis. (From Cecil Textbook of Medicine, 19th ed, p848)
A lipid cofactor that is required for normal blood clotting. Several forms of vitamin K have been identified: VITAMIN K 1 (phytomenadione) derived from plants, VITAMIN K 2 (menaquinone) from bacteria, and synthetic naphthoquinone provitamins, VITAMIN K 3 (menadione). Vitamin K 3 provitamins, after being alkylated in vivo, exhibit the antifibrinolytic activity of vitamin K. Green leafy vegetables, liver, cheese, butter, and egg yolk are good sources of vitamin K.
Ulceration of the GASTRIC MUCOSA due to contact with GASTRIC JUICE. It is often associated with HELICOBACTER PYLORI infection or consumption of nonsteroidal anti-inflammatory drugs (NSAIDS).
Products in capsule, tablet or liquid form that provide essential nutrients, such as a vitamin, an essential mineral, a protein, an herb, or similar nutritional substance. (FDA Backgrounder, June 15, 1993, p2)
A nutritional condition produced by a deficiency of VITAMIN D in the diet, insufficient production of vitamin D in the skin, inadequate absorption of vitamin D from the diet, or abnormal conversion of vitamin D to its bioactive metabolites. It is manifested clinically as RICKETS in children and OSTEOMALACIA in adults. (From Cecil Textbook of Medicine, 19th ed, p1406)
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