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  • br Conclusion br Disclosure of interest br Acknowledgement b

    2021-10-09


    Conclusion
    Disclosure of interest
    Acknowledgement
    Introduction Vitamin B6 has long been recognized as a cofactor for many enzymes, especially those involved in amino SCF, murine recombinant protein sale metabolism. Apart from its role as coenzyme, recent studies are unveiling a new role of vitamin B6 as a chemopreventive agent. High levels of vitamin B6 have been reported to suppress growth of animal or human cancer cells in vitro[1], [2], [3], [4]. Animal research also indicated that a high dietary intake of vitamin B6 suppresses herpes simplex virus type 2 transformed cell-induced tumor growth in BALB/c mice [5]. Thus, it has been considered that supraphysiological doses of vitamin B6 may have potential use in antineoplastic therapy [6]. In 1997, Slattery et al. [7] reported the case-control studies indicating an inverse association between vitamin B6 intake and colon cancer risk in the United States. This was confirmed by the case-control study in seven countries of Europe [8]. An inverse relationship between vitamin B6 intake and prostate cancer incidence has been also reported [9]. Recent case-control study has further supported an inverse association between serum vitamin B6 level and lung cancer risk [10]. Komatsu et al. [11] postulated that colorectal cancer risk might be reduced by moderate levels of dietary vitamin B6 daily consumed by humans. To test this hypothesis, they have examined effect of dietary level of vitamin B6 on the development of colon tumors in azoxymethane (AOM)-treated mice [11]. The results showed that colon tumorigenesis was significantly suppressed by moderate doses of dietary vitamin B6[11]. Thus, the preventive effect of vitamin B6 against colon carcinogenesis has important dietary consequences. This review describes recent studies on the antitumor effect of vitamin B6 and its mechanisms.
    Colon tumorigenesis Komatsu et al. [11] have studied the effect of dietary level of vitamin B6 on AOM-induced colon tumorigenesis in mice. Mice were fed the diets containing 1, 7, 14 or 35 mg pyridoxine (PN) HCl/kg for 22 weeks, and given a weekly injection of AOM for the initial 10 weeks. One hour before termination, 5-bromo-2′-deoxyuridine (BrdU) was given by injection for immunohistochemical analysis of cell proliferation. A 1 mg PN HCl/kg diet has been reported to be the minimum level required for preventing growth depression caused by vitamin B6 deficiency [12]. Supplementation of vitamin B6 caused no influence on the food intake and growth. Supplemental dietary vitamin B6 markedly suppressed the incidence of colon tumors (Fig. 1) and the number of colon tumors compared with the 1 mg PN HCl/kg diet group. Compared with the 1 mg PN HCl/kg diet, the minimum level for preventing colon tumorigenesis examined here was 7 mg PN HCl/kg diet. In general, the greatest suppression of tumorigenesis by dietary vitamin B6 was observed in the mice fed 14 and 35 mg PN HCl/kg diets. The recommended level in the AIN-93 diet is 7 mg/kg diet [13]. The optimum requirement of PN HCl appears to be 14-35 mg/kg for suppression of colon tumorigenesis. Supraphysiological dose of vitamin B6 has been believed to be potentially useful for antineoplastic therapy [6]. The result, however, implies that colon carcinogenesis can be significantly reduced by moderate levels of dietary vitamin B6. In the mice fed the 35 mg PN HCl/kg diet, no toxicity symptoms were observed throughout the entire feeding period.
    Cell proliferation Cell hyperproliferation is involved in the mechanism of carcinogenesis. Komatsu et al. [11] have found that supplemental vitamin B6 reduced the BrdU-labeling index (index of cell proliferation) in the colon of mice, whereas vitamin B6 had no significant effect on colonic epithelium apoptosis. The labeling index in all of the colon epithelium of the 14 and 35 mg PN HCl/kg diet groups was significantly lower than that of the 7 mg PN HCl/kg diet group. The labeling index of proliferating cells in all of the colon epithelium significantly correlated with the number of tumors. The labeling indices of c-myc and c-fos proteins (oncogene products relating to cell proliferation) in the colonic crypts were also significantly reduced by supplemental vitamin B6. The results imply that lowered cell proliferation by dietary vitamin B6 leads to its antitumor effect (Fig. 2).