The effect of vitamin B-6 (VB6) deficiency in mice on host susceptibility to primary and secondary Moloney-sarcoma virus (MSV)-induced tumor growth, cytotoxic activities of T cells, antibodies and natural killer (NK) cells, and phagocytosis by macrophages was examined. Five- to six-week old female C57B1/6 mice were fed 20% casein diets with pyridoxine (PN) added at 7 (PN-7), 1 (PN-1), 0.5 (PN-0.5), 0.1 (PN-0.1), or 0 (PN-0) mg per kg diet, which represent 700, 100, 50, 10, and 0% of the VB6 requirement of mice adequate for both growth and reproduction, for 4-5 weeks prior to MSV challenge and throughout the period of tumor development or immunologic testing. Animals fed PN-0.1 and -0 diets developed deficiency signs including significantly lower body weight, denuding of the snout, skin irritation and elevated excretion of xanthurenic acid before as well as after tryptophan loading. VB6 deficiency resulted in significant enhancement of tumor susceptibility. Following MSV/MSB challenge, total incidence of MSV/MSB/splenic tumors was 2/11, 1/11, 4/10, and 8/11 in mice fed PN-1, -0.5, -0.1, and -0 diets, respectively. In response to challenge with P815 mastocytoma cells, primary splenic and peritoneal T cell-mediated cytotoxicity (CMC) was significantly reduced in animals fed PN-0 or -0.1 diet. Mice fed PN-0 diet also showed significantly suppressed secondary T CMC of splenic and peritoneal lymphocytes against P815 tumor cells. Complement-dependent antibody-mediated cytotoxicity against P815 tumor cells, phagocytosis of sheep red blood cells by macrophages, and native and interferon-induced NK cell cytotoxicity against YAC tumor cells were not affected by lack of VB6. The percentage of macrophages present in the peritoneal exudate cells was increased in animals fed PN-0 diet. Immune responses were not enhanced or altered by the excess intake of VB6 (PN-7). The present studies which showed compromised host resistance to MSV oncogenesis and altered T cell cytotoxicity in VB6 deficiency provided practical information on the impaired host defense mechanism by inadequacy resulting from VB6. / Graduation date: 1984

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