Vitamin experimental

There is no record of pantothenic acid deficiency in humans, since all food contains sufficient quantities of this vitamin. Experimentally, however, neurological, gastrointestinal, and cardiovascular symptoms result from a diet lacking in pantothenic acid. 

Requirements for energy, protein, carbohydrates, Hpids, vitamins and minerals have been determined for the species commonly cultured (9). As a rule of thumb, trout and salmon diets will, if consumed, support growth and survival in virtually any aquaculture species. Such diets often serve as the control against which experimental diets are compared. 

Pure selenium deficiency, without concurrent vitamin E deficiency, is not generally seen except in animals on experimental diets (113). In China, selenium deficiency in humans has been associated with Keshan disease, a cardiomyopathy seen in children and in women of child-bearing ages, and Kashin-Beck disease, an endemic osteoarthritis in adolescents (113). 

Research lea ding to the discovery of vitamin C began in 1907 when it was observed by Axel Holst and Theodor Ern hlich that guinea pigs were as susceptible to scurvy as humans and that the disease could be produced experimentally in these animals (8). These findings led to the development of an assay for the biological deterrnination of antiscorbutic activity of food products (9). 

To find the empirical formula of vitamin C from the data in Example F.l we must express the ratios of numbers of atoms as the simplest whole numbers. First, we divide each number by the smallest value (3.41), which gives a ratio of 1.00 1.33 1.00. Molecules contain only whole numbers of atoms, and one of these numbers is still not a whole number. Hence, we must multiply each number by the correct factor so that all numbers can be rounded off to whole numbers. Because 1.33 is Vi (within experimental error), we multiply all three numbers by 3 to obtain 3.00 3.99 3.00, or approximately 3 4 3. Now we know that the empirical formula of vitamin C is C3H403. 

In experimental animals, vitamin E deficiency results in resorption of femses and testicular atrophy. Dietary deficiency of vitamin E in humans is unknown, though patients with severe fat malabsorption, cystic fibrosis, and some forms of chronic fiver disease suffer deficiency because they are unable to absorb the vitamin or transport it, exhibiting nerve and muscle membrane damage. Premamre infants are born with inadequate reserves of the vitamin. Their erythrocyte membranes are abnormally fragile as a result of peroxidation, which leads to hemolytic anemia. 

Vitamin C occurs as L-ascorbic acid and dihydroascorbic acid in fruits, vegetables and potatoes, as well as in processed foods to which it has been added as an antioxidant. The only wholly undisputed function of vitamin C is the prevention of scurvy. Although this is the physiological rationale for the currently recommended intake levels, there is growing evidence that vitamin C may provide additional protective effects against other diseases including cancer, and the recommended dietary allowance (RDA) may be increased in the near future. Scurvy develops in adults whose habitual intake of vitamin C falls below 1 mg/d, and under experimental conditions 10 mg/d is sufficient to prevent or alleviate symptoms (Bartley et al., 1953). The RDA is 60 mg per day in the USA, but plasma levels of ascorbate do not achieve saturation until daily intakes reach around 100 mg (Bates et al., 1979). Most of the ascorbate in human diets is derived from natural sources, and consumers who eat five portions, or about 400-500 g, of fruits and vegetables per day could obtain as much as 200 mg of ascorbate. 

In addition to vitamin C and vitamin E as effective blocking agents, there are other substances which also are capable of preventing nitrosamine formation which are present in normal foods. The influence of this factor on the design of experimental studies should not be overlooked. 

The longitudinal effects of experimental vitamin E deficiency on visual function in the rat have been studied by Goss-Sampson et al. (1992). After 12 months of deficiency, visual function as assessed by electroretinography was absent or grossly abnormal. This was associated with... 

Chester, J.F., Gaissert, H.A., Ross, J.S. and Malt, R.A. (1986). Augmentation of 1,2 dimethylhydrazine-induced colon cancer by experimental colitis in mice role of dietary vitamin E. J. Natl Cancer Inst. 76, 939-942. 

Ascorbic acid (vitamin C) depletion is the most consistent evidence of compromised antioxidant status in diabetes with reports of reduced levels and altered metabolic turnover in several tissues in experimentally induced diabetes in animals (Rikans, 1981 Yew, 1983 McLennan et al., 1988) and in patients with diabetes (Som et al., 1981 Jennings et al., 1987 Sinclair et al., 1991). 

The above-described experiments, calculations, and theroretical considerations showed that there is no theoretical or experimental evidence whatsoever for the 5a-C-centered radical 10. All relevant reactions can be traced back to occurrence and reactions of o-QM 3 as the central intermediate. The three reactions commonly cited to support the occurrence of the chromanol methide radical 10 in vitamin E chemistry (Figs 6.6-6.8) are actually typical processes of the o-QM intermediate (Figs 6.9-6.11). 

Reports of lead-nutrient interactions in experimental animals have generally described such relationships in terms of a single nutrient, using relative absorption or tissue retention in the animal to index the effect. Most of the data are concerned with the impact of dietary levels of calcium, iron, phosphorus, and vitamin D. These interaction studies are summarized in Table 2-12. 

Gerster, H. 1995. Carotene, vitamin E and vitamin C in different stages of experimental carcinogenesis. EurJ Clin Nutr 49 155-168. 

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