Zugl.: Giessen, Universiẗat, Diss., 1991.

The effect of dietary glycosylated vitamin B-6 on the bioavailability of vitamin B-6 was determined in 4 women. A 44-d metabolic-balance diet study was divided into a preliminary 8-d adjustment period followed by two 18-d experimental periods. The subjects were divided into two groups in a crossover design to compare the effect of low- and high-glycosylated vitamin B-6 diets on the bioavailability of vitamin B-6. The total vitamin B-6 content in the low- and high-glycosylated vitamin B-6 diets was 1.506 mg (8.91 nmol) and 1.897 mg (11.22 μmol), respectively, in which 11 and 22% was the glycosylated form, respectively. Daily 24-h urine specimens were collected by each subject throughout the study; 7- or 8-d fecal collections were made at the end of each experimental period. The four subjects' mean urinary total vitamin B-6 excretion during the low- and high-glycosylated vitamin B-6 periods was 0.76 ± 0.20 and 0.67 ± 0.06 μmol/24 h, respectively; fecal total vitamin B-6 excretion was 2.98 ± 0.43 and 4.56 ± 0.87 μmol/24 h, respectively. Expressed as % of total vitamin B-6 intake, the mean urinary total vitamin B-6 excretion was lower during the high-glycosylated vitamin B-6 period (6.0 ± 0.8%) than during the low-glycosylated vitamin B-6 period (8.5 ± 2.4%); in contrast, their mean fecal vitamin B-6 excretion during the high-glycosylated vitamin B-6 period (40.7 ± 8.2%) was greater than the low-glycosylated vitamin B-6 period (33.6 ± 5.4%). In addition, approximately 11% of ingested glycosylated vitamin B-6 was excreted in urine. These results suggest that dietary glycosylated vitamin B-6 is not completely bioavailable to humans, and the extent of its utilization is not affected by dietary glycosylated vitamin B-6 intake. / Graduation date: 1993

Recent studies in men have shown plasma levels of vitamin B-6 and pyridoxal 5'-phosphate (PLP), the active form of vitamin B-6, to increase with exercise. It was hypothesized that muscle glycogen phosphorylase might be the source of these increases as this enzyme has been shown to increase with increasing vitamin B-6 (B6) intake in the rat, seemingly to store PLP. The investigation was designed to study the effects of diet-altered glycogen stores and B6 supplements on B6 metabolism during controlled strenuous exercise. The effect of exercise (EX) on the excretion of 4-pyridoxic acid (4PA), the major B6 urinary metabolite, was also studied. The study consisted of three experimental weeks during which carbohydrate (CHO)-modified diets were fed and six EX tests were administered (one each Wednesday and Saturday). Four trained male cyclists (20-23 years) served as subjects. Week 1 a normal CHO diet was fed (NC diet, 40% of total kilocalories as CHO). During week 2, which began 7 days after week 1, a low CHO diet was fed Sunday through Tuesday (LC diet, 11% CHO) to deplete muscle glycogen. In the same week, the LC diet was followed by a high CHO diet (HC diet, 71% CHO). The HC diet was fed Wednesday through Saturday to replete, or load, glycogen stores. The NC, LC, and HC diets contained 1.64, 1.55, and 1.82 mg of B6, respectively. Week 3, beginning 14 days after week 2, was identical to week 2, but with the daily addition of an 8 mg supplement of pyridoxine. Daily exercise was encouraged Sunday through Tuesday to facilitate glycogen depletion. The EX test consisted of 50 min of continuous bicycle ergometer exercise (30 min at 60% HRmax (maximal heart rate), 15 min at 80% HRmax, and 5 min at 90% HRmax). Blood samples were drawn prior to the exercise test (pre), 2 min prior to the 90% HR max interval (during), immediately post EX (post), 30 min post, and 60 min post EX. Plasma samples were analyzed for PLP, PB6, creatine kinase (a muscle enzyme), and hematocrit and hemoglobin. Urine was collected in 24 hour aliquots and analyzed for 4PA and creatinine. The HC diet was associated with significantly lower pre exercise PB6 and PLP levels than LC diet. This was attributed to the high CHO content of HC. Increased plasma PLP and PB6 levels (pre versus post) were seen for all EX tests. This was significant for PB6 levels of all EX tests. Exercise following LC resulted in smaller pre to post increases in PB6 and PLP than other unsupplemented EX tests, but this was significant only for EX following LC versus NC(Wed). Supplementation resulted in greater pre to post increases in PLP and PB6 than EX following unsupplemented diets, but this was significant only for LC versus LC+B6. Plasma PLP and PB6 levels dropped throughout the 60 min post EX period. The 60 min post PLP levels were significantly below pre for the EX tests following diets NC(Wed), LC, HC+B6. Neither plasma volume percent (%) changes (calculated from hematocrit) nor creatine kinase % changes correlated significantly with % changes in PB6 and PLP. Urinary 4PA was elevated on all EX test days as compared to non-test days, except for EX following LC. Tissue redistribution of B6 appears to be occurring with exercise. With the LC diet, more B6 is needed for increased amino acid catabolism in the liver. In this situation tissue redistribution was not associated with increased conversion of B6 to 4PA. Greater increases in PLP with EX following supplementation suggests increased storage may have occurred. These findings are supportive of the hypothesis that increased PLP levels with exercise may originate from PLP bound to phosphorylase. The need for supplemental B6 for the athlete was not established, as status was adequate with normal intakes. / Graduation date: 1983

Oral contraceptive (OC) users frequently have lower vitamin B₆ status than non-oral contraceptive (NOC) users. However, normal dietary intake, a possible factor, has not been adequately studied. Therefore, 26 OC users and 25 NOC users, of college age, were compared with respect to dietary intake of vitamin B₆ and blood vitamin B₆ levels. OC users had been taking "the pill" for at least five months and NOC users had not taken any estrogen-progestin hormones for at least five months. A 72-hour continuous dietary intake record, kept by each subject, was used to calculate intakes of vitamin B₆ and nine other nutrients. Subjects consumed self-selected diets and none had used vitamin B₆ supplements within two weeks of this study. Intakes of all nutrients studied were comparable between the two groups. The mean intakes exceeded the recommended dietary allowance (RDA) for all nutrients except iron, calories and vitamin B₆. The mean intake of vitamin B₆ (1.4 [plus or minus] 0.5 mg/day for OC and 1.6 [plus or minus] 0.5 mg/day for NOC) did not differ significantly between the two groups. The RDA for this age group is 2.0 mg/day of vitamin B₆. The mean protein intakes were not significantly different for OC versus NOC users (72.6 [plus or minus] 19.4 g/day for OC and 66.9 [plus or minus] 13.6 g/day for NOC). The ratio of vitamin B₆ to protein was calculated for each subject. Mean ratios were 0.020 [plus or minus] 0.004 for OC and 0.025 [plus or minus] 0.01 for NOC users. This difference was significant at p<0.05. The mean ratio for both groups exceeded 0.019, which is considered to be adequate. Fasting blood samples were collected during the luteal phase (NOC) or after seven days of the pill cycle for 0C users. These samples were analyzed for whole blood and plasma (by Lind, 1980) vitamin B₆, using a microbiological assay (S.uvarum). These values were used to calculate vitamin B₆ levels in the red blood cell (RBC). A significant difference (p [less than or equal to] 0.05) was found between the mean level of RBC vitamin B₆ in the 0C users versus the NOC (12.4 [plus or minus] 5.4 ng/ml for 0C and 16.8 [plus or minus] 8.5 ng/ml for NOC). Plasma vitamin B₆ concentrations were also significantly different between the two groups. The mean ratio of plasma vitamin B₆ to RBC vitamin B₆ was not statistically different between 0C and NOC users. A questionnaire was used to compare the subject groups with respect to exercise, alcohol intake, general health, general vitamin B₆ intake and other indices. With the exception of alcohol intake, the mean scores for both groups, from this questionnaire, were similar. 0C users had a significantly higher intake of alcohol than NOC users, as measured by the questionnaire. However, the actual alcohol intake from the dietary record did not differ statistically between the two groups. The lack of a significant difference in vitamin B₆ intake, coupled with significantly different blood vitamin B₆ levels for 0C versus NOC users, tends to indicate that the 0C may be altering vitamin B₆ metabolism. Estrogens may cause a redistribution of vitamin B₆ in various body pools, with the vitamin leaving the blood and entering other tissues. Blood levels are generally used to determine vitamin status. By this assessment, 0C users have a lower vitamin B₆ status than controls. It is recommended that 0C users be encouraged to consume at least 2.0 mg/day of vitamin B₆ in their normal diets. / Graduation date: 1981

The purpose of this study was, first, to investigate whether there is a vitamin B-6 requirement for carnitine synthesis and, second, to investigate the effect of fasting on vitamin B-6 metabolism. An experimental group of 72 rats (6 per group) were fed either a vitamin B-6 deficient diet (-B6) (ad libitum, meal-fed) or a control diet (+B6) (ad libitum, pair-fed). These diets were fed for 6 weeks and then the rats were repleted with the control diet for 2 weeks. The animals were fasted for 3 days before and after repletion. Total acid soluble carnitine (TCN) and free carnitine (FCN) levels were compared in the plasma, liver, skeletal muscle, heart muscle and in the urine of rats fed +B6 diet and -B6 diets. The concentrations of pyridoxal 5'-phosphate (PLP) in the plasma, liver, skeletal muscle, and heart muscle and urinary 4-pyridoxic acid (4-PA) excretion were compared in rats fed the +B6 or -B6 diet. Similar comparisons were made in fasted and non-fasted rats. Also, plasma glucose, liver glycogen, and free fatty acid concentrations were compared. In rats fed the -B6 vs +B6 diet, the TCN concentration was significantly (P < 0.05) lower in the plasma, skeletal muscle, heart muscle and urine. With fasting, the liver TCN concentration of -B6 rats was also significantly lower than that of +B6 rats. After the -B6 rats were repleted with the +B6 diet, the TCN concentrations in the plasma, liver, skeletal muscle, heart muscle, and urine returned to those of the control rats. Thus, the decrease in TCN and FCN concentrations, and the increase of these concentrations after repletion provides evidence for a vitamin B-6 requirement in the biosynthesis of carnitine. Fasting resulted in increased concentrations of PLP in the plasma, liver, and heart muscle of rats fed a -B6 diet. The urinary 4-PA excretion of -B6 rats also increased with fasting. These changes are consistent with a redistribution of vitamin B-6 (as PLP) when there is a caloric deficit. Thus, with fasting, PLP is supplied by an endogenous source, possibly skeletal muscle glycogen phosphorylase. In -B6 vs +B6 rats, liver glycogen concentration was higher and plasma FFA concentration was lower. / Graduation date: 1987

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

This investigation was designed to add to present understanding of vitamin B-6 (B6) metabolism during exercise. Ten women, 5 aerobically trained and 5 untrained, were fed 4 controlled diets: a moderate carbohydrate (49%) (MCHO) for 2 weeks, a high carbohydrate (63%) (HCHO) for one week, MCH0+B6 for 2 weeks, and HCH0+B6 for 1 week. A one week MCHO diet separated the non-supplemented (2.3 mg B6) and supplemented (10.3 mg B6) diets. The V02 max of each subject was determined prior to the study. An exercise test was completed on day 5 or 6 of weeks 2, 3, 6, and 7. The test consisted of 20 minutes of cycle ergometer exercise at 80% V02 max, preceded by 10 minutes of warm-up and followed by a 5-10 minute active recovery. Blood samples were collected pre exercise (pre), 2-3 minutes post (post), 30 minutes post (p30), and 60 minutes post (p60) exercise. Samples were analyzed for plasma vitamin B-6 (PB6), hematocrit, and hemoglobin. Urine was collected daily in 24-hr aliquots and samples were analyzed for 4-pyridoxic acid (4PA) and creatinine. For all diets, exercise resulted in a significant increase in PB6 from pre to post and a significant decrease from post to p60, the magnitude of the change being greater with supplementation. PB6 fell below pre levels by p60 for all exercise sessions. 4PA increased significantly from the day before exercise to the day of exercise on all diets. There was no significant effect of dietary carbohydrate on levels of PB6 or excretion of 4PA. ANOVA showed no difference between the groups for PB6 or 4PA, though the trained group had lower PBS and greater 4PA excretion throughout the study despite the controlled intake. Tissue redistribution of B6 seems to occur with exercise. The increased magnitude of change in PB6 with exercise after supplementation suggests an increased storage of the vitamin, most likely associated with glycogen phosphorylase in the muscle. Trained women may have lower levels of PB6 and greater 4PA excretion as the result of a regular exercise program. However, supplementation with B6 cannot be recommended since the status of all subjects was adequate with the diet fed. / Graduation date: 1985

The bioavailability of vitamin B-6 from four selected foods was investigated in five men, aged 22 to 25 years, who were receiving a pyridoxine supplement. The subjects received a constant diet containing 1.34 mg of vitamin B-6 throughout this five-week study, except on Saturdays and Sundays when they ate their self-chosen diets. Starting on day 6 of week 1, following a five-day adjustment period, the subjects received orally 5-mg crystalline pyridoxine supplement daily, except on Tuesday and Thursday of each week. On these two days, the subjects were given orally 0 mg or 2 mg of crystalline pyridoxine, or test doses of bananas, filberts, soybeans and beef which contained around 2 mg of vitamin B-6. Vitamin B-6 was determined by microbiological assay with Saccharomyces uvarum. Vitamin B-6 bioavailability in the test food was determined by comparing 24-hour urinary total vitamin B-6 in response to the test food doses to that excreted following a 2-mg crystalline pyridoxine dose in each subject. Compared to the 100 percent bioavailability of the 2-mg crystalline PN dose, the average vitamin B-6 bioavailability in bananas was 115 + 32% and that in filberts, soybeans and beef was 93 + 8%, 73 + 20% and 87 + 7%, respectively. The metabolism of vitamin B-6 in pyridoxine-supplemented subjects was also investigated by measuring changes in plasma total vitamin B-6 which increased and was stablized after three weeks of pyridoxine supplementation. It was concluded that urinary total vitamin B-6 in pyridoxine-supplemented subjects can be used as a measure of vitamin B-6 bioavailability from test food doses. / Graduation date: 1983

Pyridoxal phosphate is a coenzyme in about 50 known enzymatic reactions. A simple and accurate method for the determination of pyridoxal phosphate would be desirable because it could provide a means to assess the nutritional status of vitamin B₆ in the human. The cyanohydrin methods to determine pyridoxal phosphate appear to be simple and promising. Cyanohydrin methods have been devised by Bonavita and Scardi, and Bonavita, and applied to biological materials by Yamada et al. The cyanohydrin procedure of Yamada et al. was investigated. In this procedure, the pyridoxal phosphate and pyridoxal in a deproteinized sample are separated with the use of a column of SM-cellulose (1 gm., equilibrated with 0.01 N acetic acid). Pyridoxal phosphate is eluted from SM-cellulose with 0.01 N acetic acid, and pyridoxal is eluted with 0.1 M sodium phosphate buffer, pH 7.4. Pyridoxal phosphate and pyridoxal are converted to their respective cyanohydrin derivatives by reaction with potassium cyanide. These cyanohydrin derivatives are measured fluorometrically at their activation and fluorescence maxima. In preliminary studies on the procedure by Yamada et al., the activation and fluorescence spectra of the cyanohydrin derivatives of pyridoxal phosphate and pyridoxal were obtained to determine the appropriate activating and fluorescent wavelength settings to use for subsequent fluorometric analyses. Pyridoxal phosphate cyanohydrin at pH 3.8 in 0.2 M sodium phosphate buffer had an activation maximum at 325 mμ and a fluorescence maximum at 415 mμ; and pyridoxal cyanohydrin at pH 10 in 0.2 M sodium phosphate buffer had an activation maximum at 355 mμ and a fluorescence maximum at 435 mμ. To obtain maximum fluorescence of the cyanohydrin derivatives, pyridoxal phosphate had to be reacted with potassium cyanide at 50°C for 60 minutes, and pyridoxal had to be reacted for 150 minutes. Following these preliminary studies, the elution pattern of pyridoxal phosphate and pyridoxal from a column of SM-cellulose was investigated. Pyridoxal phosphate was eluted with 0.01 N acetic acid; and pyridoxal, with both 0.01 N acetic acid and 0.1 M sodium phosphate buffer, pH 7.4. The recovery of pyridoxal phosphate from SM-cellulose was 93.5% when pyridoxal phosphate alone was applied to the column, and that of pyridoxal was 108.8% when pyridoxal alone was applied. When a mixture of pyridoxal phosphate and pyridoxal was applied to SM-cellulose, the recovery of pyridoxal phosphate was 105.5% and that of pyridoxal was only 59.8%. When either standard alone was added to blood, the recovery of pyridoxal phosphate in blood from SM-cellulose was 85.0%, and that of pyridoxal was only 29.1%. When a mixture of pyridoxal phosphate and pyridoxal was added to blood, the recovery of pyridoxal phosphate in blood from SM-cellulose was 62.6%, and that of pyridoxal was 52.1%. This lower recovery of pyridoxal phosphate in blood was due mainly to the high readings of the blanks. This higher recovery of pyridoxal phosphate in blood may be explained by the low concentration of pyridoxal in the buffer fractions from a column of SM-cellulose to which a mixture of pyridoxal phosphate and pyridoxal had been applied that was used to calculate the recovery. Determining the recovery of standards added to the supernatant after the precipitation of the proteins in blood, rather than to the hemolyzed blood before precipitation, would indicate whether pyridoxal phosphate and pyridoxal were lost by adsorption on the protein precipitate. The modified procedure of Yamada et al. is not sensitive enough to determine the pyridoxal phosphate and pyridoxal content of human blood. / Graduation date: 1968

No description available.