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Vitamin Scurvy

Many molecular diseases that have arisen in the course of evolution have been controlled in a somewhat similar manner. Human beings require many vitamins. Pellagra is an example of a vitamin deficiency disease—a molecular disease that originated through a mutation, perhaps millions of years ago, and was then cured by the heterotrophic process of eating other organisms that manufacture the vitamin. Scurvy and other avitaminoses are also diseases of this sort. It is not customary for us to admit that we have these diseases, because we treat them as a matter of habit by eating what is called a proper diet. [Pg.473]

A disease resulting from a deficiency of one or more vitamins is hypovitaminosis (if vitamin is supplied in insufficient quantity) or avitaminosis (complete lack of vitamin manifested by some biochemical processes disorder). Deficiency of vitamins was formerly one of the main causes of many diseases and deaths. Pellagra (deficiency of some B-complex vitamins), scurvy (vitamin C), beriberi (thiamine), rickets (vitamin D), pernicious anaemia associated with reduced ability to absorb vitamin Bj2 (corrinoids) and xerophthalmia (vitamin A) are now well-known diseases caused by vitamin deficiency. Excessive intake of one or more vitamins (especially of lipophilic vitamins A and D) also causes an abnormal state resulting from disturbances of biochemical processes and can lead to severe diseases known as hypervitaminosis. [Pg.348]

Our word vitamin was coined m 1912 m the belief that the substances present m the diet that prevented scurvy pellagra beriberi rickets and other diseases were vital amines In many cases that belief was confirmed certain vitamins did prove to be amines In many other cases however vitamins were not amines Nevertheless the name vitamin entered our language and stands as a reminder that early chemists recognized the crucial place occupied by amines m biological processes... [Pg.913]

In this period, the empirical healing of certain diseases by foods was estabUshed. Examples (3) were the treatment of night blindness (vitamin A deficiency) with hver ia many cultures over centuries, of beriberi (vitamin deficiency) by use of unpoHshed rice by the Japanese navy, of scurvy (vitamin C deficiency) by citms fmits ia the British navy or piae needle extracts by North American natives, and pellagra (niacia deficiency) by a dietary shift away from corn-based foods ia many countries. Other, nondietary empirical treatments iavolved, eg, exposure of children ia northern latitudes to sunlight to cute tickets (vitamin D deficiency) (4). [Pg.3]

The first clues to the treatment of scurvy occurred in 1535—1536 when Jacques Cartier, on advice from Newfoundland Indians, fed his crew an extract from spmce tree needles to cure an epidemic. Various physicians were recommending the use of citms fmits to cure scurvy in the mid-sixteenth century. Two hundred years later, in 1753, it was proved by Dr. James Lind, in his famous clinical experiment, that scurvy was associated with diet and caused by lack of fresh vegetables. He also demonstrated that oranges and lemons were the most effective cure against this disease. In 1753, inM Treatise on the Scurvy[ Lind pubhshed his results and recommendations (7). Eorty-two years later, in 1795, the British Navy included lemon juice in seamen s diets, resulting in the familiar nickname "limeys" for British seamen. Evidence has shown that even with undefined scorbutic symptoms, vitamin C levels can be low, and can cause marked diminution in resistance to infections and slow healing of wounds. [Pg.10]

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). [Pg.10]

Mobilization and Metabolism. The total ascorbic acid body pool in healthy adults has been estimated to be approximately 1.5 g, which increases to 2.3—2.8 g with intakes of 200 mg/d (151—158). Depletion of the body pool to 600 mg initiates physiological changes, and signs of clinical scurvy are reported when the body pool falls below 300 mg (149). Approximately 3—4% of the body pool turns over daily, representing 40—60 mg/d of metabolized, or consumed, vitamin C. Smokers have a higher metaboHc turnover rate of vitamin C (approximately 100 mg/d) and a lower body pool than nonsmokers, unless compensated through increased daily intakes of vitamin C (159). The metaboHsm of ascorbic acid varies among different species. [Pg.22]

Scurvy results from a dietary vitamin C deficiency and involves the inability to form collagen fibrils properly. This is the result of reduced activity of prolyl hydroxylase, which is vitamin C-dependent, as previously noted. Scurvy leads to lesions in the skin and blood vessels, and, in its advanced stages, it can lead to grotesque disfiguration and eventual death. Although rare in the modern world, it was a disease well known to sea-faring explorers in earlier times who did not appreciate the importance of fresh fruits and vegetables in the diet. [Pg.178]

In addition to the hazards of weather, participants in early polar expeditions often suffered from scurvy, caused by a dietary vitamin C deficiency. [Pg.772]

Schiffbase, 1147 Scurvy vitamin C and, 772 sec-Butyl group, 84 Second-order reaction, 363 Secondary alcohol, 600 Secondary amine, 917 Secondary carbon, 84 Secondary hydrogen. 85 Secondary structure (protein), 1038-1039... [Pg.1314]

Vitamin C, industrial synthesis of, 773 molecular model of, 772 scurvy and. 772 uses of. 772... [Pg.1318]

The complex series of events in collagen maturation provide a model that illustrates the biologic consequences of incomplete polypeptide maturation. The best-known defect in collagen biosynthesis is scurvy, a result of a dietary deficiency of vitamin C required by... [Pg.38]

Silk fibroin and collagen illustrate the close linkage of protein stmcture and biologic function. Diseases of collagen mamration include Ehlers-Danlos syndrome and the vitamin C deficiency disease scurvy. [Pg.39]

Peptidyl hydroxyprohne and hydroxylysine are formed by hydroxylation of peptidyl proline or lysine in reactions catalyzed by mixed-function oxidases that require vitamin C as cofactor. The nutritional disease scurvy reflects impaired hydroxylation due to a deficiency of vitamin C. [Pg.241]

The water-soluble vitamins comprise the B complex and vitamin C and function as enzyme cofactors. Fofic acid acts as a carrier of one-carbon units. Deficiency of a single vitamin of the B complex is rare, since poor diets are most often associated with multiple deficiency states. Nevertheless, specific syndromes are characteristic of deficiencies of individual vitamins, eg, beriberi (thiamin) cheilosis, glossitis, seborrhea (riboflavin) pellagra (niacin) peripheral neuritis (pyridoxine) megaloblastic anemia, methyhnalonic aciduria, and pernicious anemia (vitamin Bjj) and megaloblastic anemia (folic acid). Vitamin C deficiency leads to scurvy. [Pg.481]

Signs of vitamin C deficiency in scurvy include skin changes, fragifity of blood capillaries, gum decay, tooth loss, and bone fracmre, many of which can be attributed to deficient collagen synthesis. [Pg.496]

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. [Pg.28]

This of course goes a long way to explaining the association of scurvy with vitamin C deficiency, and the successful utilization by the British navy of lime juice as a means of prevention of the disease - hence the expression limey for British sailors. [Pg.85]

Buu Hoi and Ratsimamanga116 found that kojic acid protected the adrenal ascorbic acid in test animals during the reversible period of scurvy, without itself showing vitamin C action. [Pg.183]

Vitamin C (ascorbic acid) is probably the most known vitamin in the world. Its legendary fame is based on the two events its exceptionally important role in the treatment of scurvy and Linus Pauling s proposal to use the huge doses of ascorbic acid for the prevention of common cold. The latter proposal, based obviously on the antioxidant properties of ascorbic acid, generated numerous studies and was frequently disputed, but many people (me including) successfully apply ascorbic acid for the treatment of starting stage of common cold. [Pg.854]

The term vitamin is a misnomer, the name means vital amines, and while vitamins are essential for life they are not, as was originally supposed, amines. Most vitamins were discovered as a result of a deficiency disease produced by a restricted diet. Long voyages on sailing ships with a diet composed of ship s biscuit, dried beans, dried peas and salted meat produced scurvy. In the worst cases the whole crew were affected, but the ship s officers tended to be less severely affected. [Pg.45]

Ships that carried beer tended to be less affected than those that carried water and spirits. Presumably, the beer contained some vitamin C, possibly from the habit of dry hopping , i.e. adding a few hop cones to each barrel. Eventually, it was found that lemon or lime juice every day could prevent scurvy. The admiralty waited fifty years before they applied the discovery and then insisted that all British ships carried lime juice. [Pg.45]

June, 1912 Casimir Funk, a Polish biochemist working in London, England, wrote a review article in which he elaborated on the fact that diseases such as scurvy, beri-beri, rickets and pellagra had long been known to be associated with the dietary. Funk said that these diseases could be prevented or cured by adding certain organic substances to the diet, substances he called vitamines. 0 )... [Pg.74]

If one reads an account of the outbreak of scurvy on shipboard in the days of long voyages on sailing vessels, he finds indications of individual differences in vitamin C need. For example, in Dana s Two Years before the Mast, one member of the crew was described as suffering from severe scurvy and was about to die of the disease, while many of the crew were quite free from any symptoms. Since they had been living for the same length of time on vitamin C-deficient diets, they would, if uniformly constituted, have all been attacked at about the same time. [Pg.193]

There is, without doubt, a wide spread between the amount of vitamin C needed to prevent frank scurvy and that required for the maintenance of best health. In young growing guinea pigs about 0.5 mg. ascorbic acid per day will protect against scurvy symptoms, but there are distinct gains in health when the intakes are up to 10 times this amount.46... [Pg.194]

With respect to human beings there is some question as to what level of tissue saturation should ideally be maintained. In guinea pigs defects in developing incisors appear when the tissue concentrations are about 40 per cent of the maximum. Scurvy symptoms do not appear until the tissue saturation has reached a much lower level (about 20 per cent saturation). It seems logical to suppose that in different individuals the manifestations of mild vitamin C deficiency would be different and that a high degree of saturation would be safest from the standpoint of all the vulnerable tissues. 19... [Pg.194]

See also research, medical biochemical individuality and, 206-207 metabolism, 203 variations, exceptions and, 202 vision, 202-203 vitamin research and, 204-205 scopolamine, 228 scurvy, 167-168 self-esteem, genetics and, 16 self-selection of foods, 180 Selye, Hans, 230 senile dementia, 34-35, 227, 230 sensory physiology and psychology, 205 serotonin, 236 serum amylase, 80-81 serum lipase, 81 serum phenol sulfatase, 81 sex behavior, 100, 104-105 psychiatry and, 231 sex differences... [Pg.306]

John Hunter (1768) noted that scurvy was caused by the lack of vitamin C. He prescribed the consumption of lemon juice to treat scurvy. [Pg.395]


See other pages where Vitamin Scurvy is mentioned: [Pg.131]    [Pg.131]    [Pg.351]    [Pg.10]    [Pg.10]    [Pg.21]    [Pg.22]    [Pg.22]    [Pg.600]    [Pg.600]    [Pg.773]    [Pg.1294]    [Pg.240]    [Pg.496]    [Pg.215]    [Pg.76]    [Pg.166]    [Pg.25]    [Pg.26]    [Pg.31]    [Pg.38]    [Pg.292]    [Pg.193]   
See also in sourсe #XX -- [ Pg.279 ]




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