Erythrocytic inclusion body syndrome (EIBS) was artificially established in selected stocks of juvenile fall and spring chinook salmon (Oncorhynchus tshawytscha), chum salmon (0. keta), coho salmon (0. kisutch), Atlantic salmon (Salmo salar), and rainbow trout (0. mykiss). Adult spring chinook salmon were also artificially infected with the EIBS virus. Adult male chinook had higher prevalences of EIBS inclusion bodies than females. Cytoplasmic inclusion bodies that are associated with EIBS were not observed in steelhead (0. mykiss), brown (Salmo trutta) nor brook (Salvelinus fontinalis) trout suggesting that these stocks are less susceptible to the EIBS virus. Coho salmon with EIBS were more susceptible to Flexibacter psychrophilus, the causative agent of cold water disease (CWD) than fish without EIBS. The fish with EIBS were most susceptible to F. psychrophilus during the first 20 days after virus exposure, when inclusion bodies were most prevalent. Coho salmon infected with both the EIBS virus and F. psychrophilus required a longer recovery period than fish exposed to either pathogen alone. Most investigations of EIBS require in vivo experimentation and artificial infections using diseased fish tissues. Heterologous tissue used to establish EIBS did not contribute to anemia nor mortality. Death was not attributed to the EIBS virus alone but to the combined effects of the virus and a secondary pathogen. The severity of EIBS may be reduced with dietary Vitamin C prophylaxis. Fish fed 1,000 mg ascorbic acid/ Kg of diet had the fewest signs of EIBS; they had the highest hematocrit values and the lowest incidence of cytoplasmic inclusion bodies. However, vitamin C therapy alone was not sufficient to prevent the disease. / Graduation date: 1992

Thesis (M.S.)--University of Hawaii at Manoa, 2004. / Includes bibliographical references (leaves 67-84). Also available via World Wide Web.

Thesis (M. Phil.)--University of Hong Kong, 1972. / Typewritten.

No description available.

The influence of vitamin C on the pharmacokinetics of caffeine was investigated in ten elderly males, age 66 to 86 years. Caffeine (4 mg kg⁻¹) was administered intravenously on three different occasions over a seven-week period: before vitamin C restriction, after approximately four weeks of vitamin C restriction (15 mg dietary intake per day), and after two weeks of vitamin C supplementation (500 mg orally, twice daily). Blood and urine samples were collected over a 48-hour period following each caffeine administration. The plasma half-life (t₁/₂), rate constant of elimination (K), apparent volume of distribution (V), total body clearance (TBC), renal clearance (RC), and metabolic clearance (MC) of caffeine were determined. Simultaneous plasma (PVC), whole blood (WBVC), and leukocyte (WBCVC) vitamin C concentrations were obtained. All of the mean vitamin C values determined at the first kinetic trial (KT-1) were within the normal ranges for the respective biologic fluid or tissue. All of the mean vitamin C values changed significantly during the study; decreasing to below the normal ranges by the second kinetic trial (KT-2) following dietary vitamin C restriction, and increasing to the normal ranges by the third kinetic trial (KT-3) following vitamin C supplementation. All of the decreases and increases in the individual and average vitamin C concentrations paralleled the observed decreases and increases in the daily vitamin C intake. None of the caffeine pharmacokinetic parameters evaluated changed significantly during the study. The mean rate constant of elimination was approximately 0.15 hr⁻¹, the average plasma half-life was approximately 4.5 hours, and the mean apparent volume of distribution was approximately 500 ml kg⁻¹ for all three kinetic trials. The average total body, renal, and metabolic clearances were approximately 76.9, 1.3, and 76.0 (ml hr⁻¹)kg⁻¹, respectively, for all three kinetic trials. With the exception of V and TBC, the various pharmacokinetic characteristics investigated were in general agreement with data reported for younger subjects. The average apparent volume of distribution determined at any of the kinetic trials was about 16% lower than the value reported for young, healthy subjects. Similarly, the mean total body clearance observed was about 21% lower than that observed in young, healthy subjects. Since the average elimination rate constant observed in these elderly subjects is similar to the values observed in younger subjects and since TBC is equal to the product of V times K, the reduced TBC observed in this study appears to be due to the reduction in V, rather than to a decrease in the intrinsic metabolic capacity of the liver with aging. No relationship between vitamin C intake and/or body levels and the pharmacokinetics of caffeine was observed. These results indicate that the elimination of caffeine in the elderly is not affected significantly by the concentrations of vitamin C achieved during the study.

Ascorbic acid (AA), in popular speech vitamin C, is a commonly known nutrient. It is involved in several biological processes and deficiency can lead to scurvy. Recent publications have shown the impact of AA on epigenetic regulation in mice. Addition of AA, via enzymatic activity, enhances the generation of 5-hydroxymethylcytosine (5hmC), which is an intermediate in active demethylation of DNA. The role of AA on epigenetic changes in humans has to our knowledge never been studied. In this study, naïve CD4+ T cells from blood donors were used as a model system to investigate AAs possible role in methylation changes in the immune system. By using dot-blot assay, hydroxymethylated DNA immunoprecipitation (hmeDIP) and qPCR, changes in methylation executed by AA could be detected. A confirmation of AAs impact on epigenetic changes in mice was observed. AA enhanced the levels of 5hmC compared to untreated cells. The Jurkat cell line, a human T lymphocyte cell line, showed an opposite result. Treatment with AA decreased the levels of 5hmC compared to untreated cells. When comparing this result with the results obtained in human naïve T cells, the same observation was made. The difference between mouse and human in the ability of producing and metabolize AA could be a reason for this opposite result. Since AA had the ability to modify epigenetic changes in primary human CD4+ T cells, the results suggest that AA may have a function in the human immune system.

Graduation date: 1936

Vitamin C occurs in relatively high concentrations in fresh and processed fruits and vegetables but is found to a lesser extent in animal tissues and animal-derived products. Nearly 90 % of vitamin C in the human diet is obtained from fruits and vegetables but this can be indirect by way of commercially prepared fruit juices. These juices are often enriched with vitamin C which has been synthetically prepared. There is a wide range of such juices on the New Zealand market, and they are a significant source of dietary vitamin C for many in the population. The focus of this research is on the Keri range of juice products.The present study monitors the fate of vitamin C during storage of Keri juices up to the best-before date, and under a range of other storage and consumption situations. Two methods were adopted for determining ascorbic acid (AA, the chemical identity of vitamin C). These were the titrimetric method, which is based upon the reduction of the dye 2,6-dichlorophenolindophenol by AA in acidic solution, and liquid chromatography, which is used to separate AA from its immediate oxidation product dehydroascorbic acid. In the latter method these two analytes can be measured independently. The liquid chromatography was less successful than the simpler titrimetric method, so most of the work was done by titration. However, the concentration of dehydroascorbic acid, which has vitamin C activity in vivo, remained uncertain. Moreover, the titrimetric method could not be applied to juices with high purple anthocyanin concentrations, like blackcurrant, because the colour change at the titration end point could not be detected. pH adjustment to change colour was ineffective, and decolourisation with charcoal led to the rapid and complete destruction of AA. The concentration of AA in Keri juices at the time of manufacture were always much higher than claimed on the labels. Storage for up to nine months at room temperature resulted in a loss in AA of between 37 and 68 %, depending on the juice and exposure to fluorescent light. However, the time of storage was a much more dominant factor than light exposure. The kinetics of loss, straight lines, were most easily explained by an aerobic model of AA degradation from oxygen diffusing across the polyethylene tetraphthalate bottle wall. Overall, the label claims made were defensible in terms of the best-before date, because it took at least 100 days of storage before the AA concentration in the most susceptible juices fell below the claimed value. This is because these drinks are fast moving consumer goods and storage beyond 100 days is unlikely. (Nonetheless, the supplier (Keri Juice Company) has since adopted its new unitised method of formulating juice. This has resulted in an initially higher concentration of vitamin C as compared to the juices under investigation.) In the nine months storage experiment there was some evidence for the presence of dehydroascorbic acid in blackcurrant drinks, but not in another three juices. Pasteurisation during preparation of these drinks resulted in up to 7 % loss of AA, probably due to oxygen dissolved in water, and accelerated by heat of pasteurisation. Higher temperatures in later storage also accelerated losses. Progressive exposure of juice to air during simulated consumption of 3 L bottles over a week also accelerated losses. Finally, exposure to sunlight in a diurnal temperature environment accelerated losses five-fold higher than in total darkness. Filtration of ultraviolet light approximately halved the loss due to sunlight. Overall however, it can be concluded that AA in the Keri range of juices is very resistant to degradation of AA.

Thesis (M.S.)--University of Missouri-Columbia, 2007. / The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Title from title screen of research.pdf file (viewed Nov. 11, 2008). Includes bibliographical references.

Thesis (M.S.)--University of Michigan, 1976.