Human diseases pernicious anemia

Cobalt is one of twenty-seven known elements essential to humans (28) (see Mineral NUTRIENTS). It is an integral part of the cyanocobalamin [68-19-9] molecule, ie, vitamin B 2> only documented biochemically active cobalt component in humans (29,30) (see Vitamins, VITAMIN Vitamin B 2 is not synthesized by animals or higher plants, rather the primary source is bacterial flora in the digestive system of sheep and cattle (8). Except for humans, nonmminants do not appear to requite cobalt. Humans have between 2 and 5 mg of vitamin B22, and deficiency results in the development of pernicious anemia. The wasting disease in sheep and cattle is known as bush sickness in New Zealand, salt sickness in Florida, pine sickness in Scotland, and coast disease in AustraUa. These are essentially the same symptomatically, and are caused by cobalt deficiency. Symptoms include initial lack of appetite followed by scaliness of skin, lack of coordination, loss of flesh, pale mucous membranes, and retarded growth. The total laboratory synthesis of vitamin B 2 was completed in 65—70 steps over a period of eleven years (31). The complex stmcture was reported by Dorothy Crowfoot-Hodgkin in 1961 (32) for which she was awarded a Nobel prize in 1964. [Pg.379]

Much of the toxicological interest in cyanide relating to mammals has focused on its rapid lethal action. However, its most widely distributed toxicologic problems are due to its toxicity from dietary, industrial, and environmental factors (Way 1981, 1984 Gee 1987 Marrs and Ballantyne 1987 Eisler 1991). Chronic exposure to cyanide is correlated with specific human diseases Nigerian nutritional neuropathy, Leber s optical atrophy, retrobulbar neuritis, pernicious anemia, tobacco amblyopia, cretinism, and ataxic tropical neuropathy (Towill etal. 1978 Way 1981 Sprine etal. 1982 Beminger et al. 1989 Ukhun and Dibie 1989). The effects of chronic cyanide intoxication are confounded by various nutritional factors, such as dietary deficiencies of sulfur-containing amino acids, proteins, and water-soluble vitamins (Way 1981). [Pg.939]

One of the main difficulties in this work was that until the late 1940s the only means of assay for the active principle was to test the effect of the preparations on human patients. The disease could not be produced in animals. Patients with pernicious anemia are very sick. They also sometimes show spontaneous remissions so that monitoring the purification was extremely difficult. Nevertheless by 1945 patients were satisfactorily treated by taking less than 1 mg/day of active material compared with 400 g raw liver in 1926. [Pg.30]

Taylor studied the activity curves of all the proteinases at different pH s in various diseases of the human stomach (T18-T20). He found that in pernicious anemia, cancer of the stomach, and duodenal ulcer the activity cun es of proteolytic enzymes differed from those of normals. Only one patient exhibited a curve with two normal maxima, and the... [Pg.249]

Cobalt is found in vitamin Bn, its only apparent biological site. The vitamin is a cyano complex, but a methyl or methylene group replaces CN in native enzymes. Vitamin-Bi2 deficiency causes the severe disease of pernicious anemia in humans, which indicates the critical role of cobalt. The most common type of reaction in which cobalamin enzymes participate results in the reciprocal exchange of hydrogen atoms if they are on adjacent carbon atoms, yet not with hydrogen in solvent water ... [Pg.4]

Metal ions are required for many critical functions in humans. Scarcity of some metal ions can lead to disease. Well-known examples include pernicious anemia resulting from iron deficiency, growth retardation arising from insufficient dietary zinc, and heart disease in infants owing to copper deficiency. The ability to recognize, to understand at the molecular level, and to treat diseases caused by inadequate metal-ion function constitutes an important aspect of medicinal bioinorganic chemistry. [Pg.505]

Vitamin 5,2 (cyanocobalamin. Figure 14-9) is involved in the manufacture of the red corpuscles of the blood. It is used for the treatment of pernicious anemia, and it is perhaps the most potent substance known in its physiological activity 2 micrograms per day (2 x 10 g) of vitamin Bj2 is effective in the control of the disease. The vitamin can be isolated from liver tissue, and is also produced by molds and other microorganisms. Each molecule of vitamin B,2 contains one cobalt atom. This is the only compound of cobalt that is known to be present in the human body. [Pg.477]

Propionic acid fermentation is not limited to propionibacteria it functions in vertebrates, in many species of arthropods, in some invertebrates imder anaerobic conditions (Halanker and Blomquist, 1989). In eukaryotes the propionic acid fermentation operates in reverse, providing a pathway for the catabolism of propionate formed via p-oxidation of odd-numbered fatty acids, by degradation of branched-chain amino acids (valine, isoleucine) and also produced from the carbon backbones of methionine, threonine, thymine and cholesterol (Rosenberg, 1983). The key reaction of propionic acid fermentation is the transformation of L-methylmalonyl-CoA(b) to succinyl-CoA, which requires coenzyme B12 (AdoCbl). In humans vitamin B deficit provokes a disease called pernicious anemia. [Pg.88]

Even if you have all the iron in the world, you can still become anemic if you don t get a few micrograms of cobalt in your diet. (It s not just humans the salt licks that farmers and zookeepers put out for their animals include cobalt salts.) If you don t get enough of Bj, or the related molecule folate, you develop what is called pernicious anemia, a disease that is as bad as it sounds. Without cobalt s carbon-moving abih-ties, you can t build enough red blood cells. [Pg.126]

The coenzyme is required only in small amounts 2-5 mg is present in the average human, for example, and one of the first signs of deficiency is the failure to form red blood cells. Hence the anemia, but the disease is not treated successfully by the methods that work for the usual iron-deficiency anemia, which explains the term pernicious anemia. [Pg.498]

Although cobalt ions are found in both the (II) and (III) oxidation states, the most important biological compound of cobalt is vitamin B12 or cobalamin where the Co(III) form is present (256) (Fig. 6.10). Cobalamin or related substances are important biological compounds that are involved in a great variety of activities, particularly in bacteria. Vitamin B12 is also necessary in the nutrition of humans and probably of most animal and plant species. It is of critical importance in the reactions by which residues from carbohydrates, fats and proteins, are used to produce energy in living cells. Pernicious anemia is a severe disease in elderly people. This disease is usually accompanied in mammals by the increased excretion of methylmalonic acid in the urine. Today it is effectively controlled by a 100 /ig injection of vitamin B,2. [Pg.369]

Vitamin Bu, the antipemicious anemia factor, has the structural formula shown in Fig. 8. It is synthesized by bacteria and filamentous molds but not by animals or green plants. The vitamin was first recognized through studies of pernicious anemia, a disease in which the ability of the individual to absorb vitamin Bu is lost as a result of failure of the stomach to secrete a substance termed intrinsic factor. This substance is present in normal gastric juice and appears to be essential for the transport of vitamin B12 from dietary sources across the intestinal wall into the blood stream. Pernicious anemia is therefore the manifestation of a deficiency of vitamin Bu as caused by a failure to absorb the vitamin from the digestive tract. The disease, which occurs only in human beings, must be treated by injection of the vitamin, formerly obtained from liver extract and more recently from special fermentations. A deficiency of vitamin B12 may also arise from a lack of the substance in the diet, especially in the case of farm animals. [Pg.731]

The curative material, which is abundant in green leafy vegetables, was named folic acid. However, this name is usually reserved for the synthetic compound used in dietary supplementation. The natural forms are largely the coenzymes (Fig. 6), which are collectively called folates. The last of the accepted human vitamins to be discovered was vitamin Bn. A cobalt-containing organic compound needed in very small amounts, it cures and prevents pernicious anemia, which was often a fatal disease of people over 60 years of age. Its complex structure (Fig. 7) was determined by X-ray diffraction after numerous efforts at chemicai characterization had failed. However, cy anocobalamin, the compound isolated and the form used in nutritional supplementation, is an artifact of the isolation and synthesis. The natural vitamin may have OH in place of CN but consists largely of the coenzyme forms. [Pg.204]

Cobalamin is the anti-pernicious anemia factor. Minutest amounts (a few micrograms) cure pernicious anemia in man. The disease is characterized by a drastic decrease of the erythrocyte count (due to a disturbance in the maturation of red blood cells). Pernicious anemia does not arise from a dietary deficiency, but rather is caused by a defect in the absorption of the vitamin. Cobalamin (designated the extrinsic factor, in this connection) can be taken up by the human organism only in the presence of the intrinsic factor, a mucoprotein. The latter is formed in the gastric mucosa its absence causes pernicious anemia. [Pg.383]

Pernicious anemia most often occurs in persons over 40 years of age. It is practically unknown among black people. In England, approximately 1 of 1000 persons suffers from this disease. The World Health Organization recommends a daily dose of only 1 pg (10 g) of vitamin Bj2. Human body stores about 5 mg of the cobalamins. Neither plants nor animals can synthesize cobalamins. This vitamin is unique in that it is synthesized only by certain microorganisms, notably anaerobic bacteria. [Pg.216]

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