The purpose of this study was to examine the effects of Vitamin E deficiency and/or ionizing radiation on uterine ceroidogenesis, incisor depigmentation, serum Vitamin E, haemoglobin concentration, haematocrit, 2,3-DPG and adipose tissue fatty acid composition in rats. An attempt was also made to define the nature of ceroid and to examine its relationship to lipofuscin. Rats fed a Vitamin E deficient diet deposited increasing amounts of ceroid in the uterine musculature between 90 to 261 days after the imposition of the experimental diets. This pigment was found to be essentially similar to lipofuscin. Ionizing radiation did not have any apparent effect on the rate and degree of ceroidogenesis in Vitamin E deficient rats, althought it did cause a significant decrease in the serum Vitamin E levels of both Vitamin E deficient and supplemented animals. The serum Vitamin E of the deficient animals were significantly lower than those of the supplemented animals, irrespective of their radiation status. Vitamin E deficiency also caused a depigmentation of the maxillary incisors of the animals and had no effect on the haemoglobin concentration, haematocrit and 2,3-DPG levels of these rats. Finally, Vitamin E deficiency and ionizing radiation resulted in a decrease in the polyunsaturated fatty acid content of adipose tissues. / Education, Faculty of / Curriculum and Pedagogy (EDCP), Department of / Graduate

Thiamine is an important nutrient found in significant amounts in wheat flours. This vitamin is heat labile thus destruction occurs during bread baking. Using a kinetic approach, the effect of heat and pH on thiamine degradation in a model system were studied. In order to compare the stability of thiamine from natural (whole wheat) and synthetic (enriched white) sources, thermal destruction of thiamine in the two breads was investigated. Destruction rates of thiamine hydrochloride in phosphate buffer at pH 6.0 and temperatures between 80 and 120°C were measured. The breakdown reaction could be described by first order kinetics. An energy of activation of 34.2. kcal/mole was obtained. Destruction rates of thiamine hydrochloride in phosphate buffer at 120°C were measured for pH values between 4.0 and 7.0. The reaction rate increased as the system was made more alkaline, with greater destruction at pH 6.0 and above. Thiamine losses in an enriched white flour system baked at a nominal temperature of 246°C (475°F) for 60, 75 and 90 min were found to be 2.4, 27.9 and 29.2%, respectively. Two experiments were carried out with 450 g (1 lb) enriched white loaves baked at 221°C (430°F). Baking times were 30 min for the first experiment, and 15, 37 and 60 min for the second experiment. No appreciable thiamine destruction were found in either experiment. The main investigation was with a semi-model system of 12g bread loaves made from enriched white and whole wheat flours. Four different nominal oven temperatures of 177, 221, 246 and 288°C (350, 425, 475 and 550°F) were used with four different baking times for each run. The pH of the dough and baked bread were determined. Oven, crust and loaf center temperatures were monitored. The mass average temperature data of the bread during baking showed a changing rate of temperature rise, and because of this, it was not possible to obtain kinetic data. However, a linear relationship was obtained when the logarithm of the percent thiamine retention was plotted against time. This experiment showed a lower thiamine stability with higher oven temperature. Thiamine was less stable in whole wheat bread than in enriched white bread. This might be explained by higher pH and ash content in whole wheat bread. Thiamine losses during normal baking of whole wheat and enriched white bread were found to be in the range of 28.3 to 47.8%. / Land and Food Systems, Faculty of / Graduate

The effect of the dietary status of vitamin A on carbohydrate metabolism, postmortem isometric tension development and shear resistance of Pectoral is major muscle was studied. Depletion studies, conducted over a five week period, indicated a definite influence of vitamin A deficiency on muscle carbohydrate metabolism. Mild hypovitaminosis A induced an increase in glycogen deposition whereas a severe deficiency led to a reduction of these elevated stores. Vitamin A deficiency did not affect the abi I ity of P. major strips to develop isometric tension postmortem. P. major strips sampled from deficient cockerels generally required longer to reach maximum tension and, in the later stages, developed significantly greater maximum tension than those of controls. The extended times to maximum tension reflected an increased muscle glycogen content. A significant increase in shear value similarly corresponded to the increased myofibrillar contraction noted in the later deficiency stages. Cockerels which had previously received a completely vitamin A deficient ration for five weeks were utilized for the two week repletion study. Though there was a distinct delay in response to the feeding of a vitamin A adequate ration, the muscle glycogen content, isometric tension parameters and shear values of repleted birds were similar to those of controls within the two week period. / Land and Food Systems, Faculty of / Graduate

Typescript / M.S. Florida State College for Women 1934 / Includes bibliographical references

The lactic dehydrogenase activity in plasma and tissues was measured in the thiamine-deprived, the oxythiamine-treated and the pyrithiamine-treated rats as well as the control rats. The lactic dehydrogenase levels of brain and kidney were significantly increased by oxythiamine treatment. The enzyme activity in heart was markedly decreased only in the thiamine-deprived rats. Unlike the above tissues, the enzyme levels in liver were decreased by 29-44 per cent in all three types of thiamine deficiency, However, the enzyme activity in plasma was significantly increased only by pyrithiamine administration. The distribution patterns of lactic dehydrogenase isozymes were electrophoretically examined in these deficiencies. No significant difference among the three thiamine-deficient groups was observed in brain, kidney, and heart. All five isozymes were observed in proportions that are highly specific for the tissues involved. Two extra bands, in addition to five major bands, were found in liver. In thiamine deprivation liver LDH_3 was noticeably more abundant than LDH_2 in some cases, which is opposite to that found in the control. One extra band between LDH_2 and LDH_3 was absent in liver after pyrithiamine treatment. No noticeable difference in the isozyme distribution of plasma was found among the three thiamine-deficient groups. Blood pyruvate along with lactate was significantly increased by oxythiamine treatment. Pyrithiamine administration also caused a marked increase of blood pyruvate along with lactate only in the phase of the polyneuritic convulsion. Remarkable increases in weight of the adrenal glands were observed in all three cases.

Objectives: Vitamin D deficiency is highly prevalent and has been linked to increased morbidity and mortality. There has been an increase in testing for vitamin D with a concomitant increase in costs. While individual factors are significantly linked to vitamin D status, prior studies have not yielded a model predictive of vitamin D status or 25(OH)D levels. The purpose of this investigation was to determine if a prediction model of vitamin D could be developed using extensive demographic data and laboratory parameters. Methods: Patient data from 6 Veterans Administration Medical Centers were extracted from medical charts. Results: For the 14,920 available patients, several factors including triglyceride level, race, total cholesterol, body mass index, calcium level, and number of missed appointments were significantly linked to vitamin D status. However, these variables accounted for less than 15% of the variance in vitamin D levels. While the variables correctly classified vitamin D deficiency status for 71% of patients, only 33% of those who were actually deficient were correctly identified as deficient. Conclusion: Given the failure to find a sufficiently predictive model for vitamin D deficiency, we propose that there is no substitute for laboratory testing of 25(OH)D levels. A baseline vitamin D 3 daily replacement of 1000-2000 IU initially with further modification based on biannual testing appears to factor in the wide variation in dose response observed with vitamin D replacement and is especially important in high-risk groups such as ethnic minorities.

Using data from the Health, Aging, and Body Composition study, we examined whether low 25-hydroxyvitamin D (25[OH]D) concentrations were associated with prevalent or incident cognitive impairment. Serum 25(OH)D concentrations were measured in 2,786 older adults and categorized as <20 ng/mL, 20 to <30 ng/mL, or ≥30 ng/mL. Cognitive impairment was defined as a score >1.5 standard deviations below race and education specific means on either digit symbol substitution test or modified mini-mental state test. Logistic regression determined the odds of cognitive impairment at baseline and year 5 by 25(OH)D category. 25(OH)D concentrations were <30 ng/mL in 57.3% of whites and 84.6% of blacks. After excluding participants with baseline cognitive impairment (n = 340), 13% of whites and 13% of blacks developed cognitive impairment by year 5. In whites, 25(OH)D concentrations <30 ng/mL were not associated with prevalent or incident cognitive impairment. Black participants with 25(OH)D concentrations <20 ng/mL had a higher odds of prevalent, but not incident cognitive impairment (OR (95% CI): 2.05 (1.08–3.91), p = 0.03) compared to participants with 25(OH)D concentrations ≥30 ng/mL. Low 25(OH)D concentrations were associated with twofold higher odds of prevalent cognitive impairment in blacks.

Vitamin B6 was discovered almost 90 years ago, and since then it has received a lot of interest from the scientific community due to its role in human health and its impact on several biochemical processes. One of the most interesting aspect of vitamin B6 studied in the past decade is its role in cancer. From the research on this subject so far, the following can be suggested: early-stage cancer cells have a higher vitamin B6 content than normal cells due to its role in metabolic processes. As the cancer makes progress, there is a change in vitamin B6 activation and trapping in the cell, decreasing the amount of active vitamin B6 in the cell in order to resist cell death. From these conclusions, we can see that vitamin B6 could potentially be an interesting radiotracer to use for diagnosis and staging of cancers. One of the most predominant form of imaging which is done nowadays to detect and diagnose cancers is Positron Emission Tomography (PET) imaging. Research on PET imaging is driven by the potential of new radiotracers which can be added to the current arsenal of tools for the fight against cancer. Therefore, this project focuses on the attempted synthesis of two potential radiotracers derived from vitamin B6 based on the insertion of fluorine-18. None of the two proposed radiotracers were successfully synthesized but we successfully synthesized one cold standard and difluorinated pyridoxine with cold conditions similar to radiochemistry. The main issues which were faced were the degradation of the potential precursors when attempting fluorination, the lack of reactivity of intermediates for the formation of precursors and an acetyl migration leading to the wrong precursors. By using a milder fluorination strategy to avoid degradation (room temperature, no free fluoride source: AgF2 as fluorinating agent), the 6-Fluoropyridoxine cold standard was synthesized. By changing the protection strategy (not using any acetyl groups), acetyl migration was avoided which led to the synthesis of a difluorinated pyridoxine using mild conditions (room temperature). The difluorination was also successful using harsher conditions (heat). There is still a lot of work to do to synthesize a radiotracer derived from vitamin B6 but there are some signs that this may be possible with additional work.

Medial calcification refers to mineral deposition in the middle layer of arteries. This mineralization is common in chronic kidney disease patients and causes an increased chance of cardiovascular complications. Calcitriol, the active form of vitamin D, is often administered to these patients to treat an associated condition, secondary hyperparathyroidism. Unfortunately, calcitriol treatment may promote vascular calcification due to increasing serum calcium and phosphate. We examined the effects of calcitriol supplementation on vascular smooth muscle cell (VSMC) calcification, through atomic absorption, scanning electron microscopy, and western blot analysis. Additionally, we examined the effects of the combinations of calcitriol, fibroblast growth factor 23 (FGF-23), and klotho. We determined that calcitriol supplementation alone increased calcification but was not associated with a transition towards an osteoblast-like phenotype. On the other hand, the combination of calcitriol and FGF-23 caused a decrease in calcification, but this decrease was attenuated with the further addition of klotho.

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