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

No description available.

Serine transhydroxymethylase (STHM), a pyridoxal 5'- phosphate requiring enzyme is indirectly involved in pyrimidine deoxynucleotide metabolism. A decrease in the activity of this enzyme could lead to altered deoxycytidine (dC) metabolism. This study was undertaken to determine if a vitamin B-6 deficiency affects dC metabolism. The effect of a vitamin B-6 deficiency on the activity of STHM in liver, thymus, spleen and bone marrow was examined. In addition, the effect of a vitamin B-6 deficiency on urinary excretion of dC was examined. The effect of a vitamin B-6 deficiency on the urinary excretion and tissue retention of ³H label from ip injected ³H-dC was monitored. Rats were assigned in groups of six to one of four treatment groups: ad libitum control (ALC), pair fed control (PFC), ad libitum deficient (ALD) or meal fed deficient (MFD). At the end of weeks 2 and 6, rats from each treatment group received an ip injection of ³H-dC. Urines were collected for 24 hours following the ip inhibited due to lack of cofactor, then dTMP levels would fall. In an attempt to increase the concentration of dTMP, enzymes active in the conversion of dC and dCMP to dUMP would be expected to increase. Thus, dC salvage pathways would increase and dC synthesis would decrease as metabolism shifts toward production of deoxythymidine triphosphate (dTTP). The result would be lower urinary dC excretion. The present study was undertaken to explore the relationship between vitamin B-6 and pyrimidine deoxynucleotide metabolism. There were four hypothesis tested: Vitamin B-6 deficient rats will excrete less urinary dC than either ad libitum or pair fed controls; vitamin B-6 deficient rats will excrete a lower percentage of labeled dC in urine than control rats; vitamin B-6 deficient rats will incorporate less labeled dC into DNA than control rats but may retain more label in tissues as dC metabolites; activity of STHM from tissues of vitamin B-6 deficient rats will be lower than that from the control rats. / Graduation date: 1990

No abstract available. / Thesis (M.Sc.)-University of Durban-Westville, 1990.

The problem of this study is to determine the vitamin B-6 status of patients who have chronic obstructive pulmonary disease (COPD). Erythrocyte aspartate transaminase assay was the method for measuring vitamin B-6 status. The vitamin B-6 status was examined in thirty subjects (ten COPD subjects and twenty control subjects). An unpaired t-test was used to compare the vitamin B-6 status of the COPD group versus the control group. Four determinants (percentage stimulation, ratio of basal to stimulated activity, basal activity, and stimulated activity) were used to determine vitamin B-6 status in both groups of subjects. Percentage stimulation and ratio of basal to stimulated activity were not significantly different (control group versus COPD group) at the .05 level. However, two of ten COPD subjects had values for percentage stimulation that were two standard deviations above the mean, indicating a poor B-6 status. In contrast, basal activity and stimulated activity of erythrocyte aspartate transaminase were found to be significantly lower at the .05 level in the COPD group than the control group. Therefore, the COPD subjects as a group had some biochemical characteristics of a lower level of vitamin B-6 than the controls.