Although many epidemiological studies indicate protective effect of vitamin C against a variety of human malignancies its mechanism(s) of action is questionable. The presented results show that the part of its effect may be accomplished by mononuclear cells, as necessary participants in body defence. Namely, in a long-term in vitro assay we tested vitamin C influence on random migration ability of malignant pleural effusion mononuclears (PEM) obtained from breast cancer patients. Vitamin C in a dose- (50-500 micrograms) and time-dependent (4-44 h) manner inhibited PEM motility, suggesting that immobilization of cells in situ may contribute to its beneficial effect in human cancers.
Epidemiologic evidence for vitamin C and vitamin E in cancer prevention.
Am J Clin Nutr, 1995 Dec, 62:6 Suppl, 1385S-1392S
Antioxidant nutrients have been hypothesized to be protective against cancer. Vitamin C is a major circulating water-soluble antioxidant, and vitamin E is a major lipid-soluble antioxidant. Many case-control and cohort studies have related cancer risk to estimates of nutrient intake derived from food intake reports. Diets high in fruit and vegetables, and hence high in vitamin C, have been found to be associated with lower risk for cancers of the oral cavity, esophagus, stomach, colon, and lung. Diets high in added vegetable oils, and hence high in vitamin E, have been less consistently shown to be associated with cancer protection. This may be because vitamin E offers less protection against cancer or because the estimation of vitamin E intake is less accurate than is the estimation of vitamin C intake. In contrast with the findings from epidemiologic studies based on foods, observational studies of nutrients consumed in supplements and recent experimental trials provide little support for a strong protective role for vitamins C or E against cancer. If vitamins C or E are indeed protective against cancer, that protection may derive from their consumption in complex mixtures with other nutrients and with other bioactive compounds as found in the matrix provided by whole foods.
Effect of vitamin C on prostate cancer cells in vitro: effect on cell number, viability, and DNA synthesis.
Prostate, 1997 Aug, 32:3, 188-95
BACKGROUND: Many studies describe the protective role of vitamin C (ascorbic acid) against cancer development and in treatment of established cancer. The present study investigated whether ascorbic acid demonstrates a therapeutic benefit for prostate cancer. METHODS: Androgen-independent (DU145) and androgen-dependent (LNCaP) human prostate cancer cell lines were both treated in vitro with vitamin C (0-10 mM). Cell counts, cell viability, and thymidine incorporation into DNA were determined. RESULTS: Treatment of DU145 and LNCaP cells with vitamin C resulted in a dose- and time-dependent decrease in cell viability and thymidine incorporation into DNA. Vitamin C induced these changes through the production of hydrogen peroxide; addition of catalase (100-300 units/ml), an enzyme that degrades hydrogen peroxide, inhibited the effects of ascorbic acid. Superoxide dismutase, an enzyme that dismutates superoxide and generates hydrogen peroxide, did not prevent decreases in cell number and DNA synthesis, suggesting further the involvement of hydrogen peroxide in vitamin C-induced changes. These results clearly indicate that reactive oxygen species (ROS) are involved in vitamin C-induced cell damage. However, that singlet oxygen scavengers such as sodium azide and hydroquinone and hydroxyl radical scavengers such as D-mannitol and DL-alpha-tocopherol did not counteract the effects of ascorbic acid on thymidine incorporation suggests that vitamin C-induced changes do not occur through the generation of these ROS. CONCLUSIONS: Vitamin C inhibits cell division and growth through production of hydrogen peroxide, which damages the cells probably through an as yet unidentified free radical(s) generation/mechanism. Our results also suggest that ascorbic acid is a potent anticancer agent for prostate cancer cells.
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