Cobalt deficiency symptoms

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. 

The toxicological significance of the chemical form does not only derive from the fact that the great majority of the elements in the periodic table are metals and metalloids many metals also make it possible to demonstrate the dose-effect relationship very clearly. Copper, manganese, selenium, cobalt and zinc, for example, are essential trace elements whose absence inevitably results in deficiency symptoms or loss of proper functioning. On the other hand, large doses are cytotoxic or cause cancer. 

Cobalt Meat, Uver, dairy foods Component of vitamin B12 Pernicious anemia (vitamin-deficiency symptom)... 

Sheep, cattle, and goats are the only species in which cobalt deficiency has been observed. Horses and pigs develop normally in the naturally occurring cobalt-deficiency areas, and rats and rabbits remain free from any evidence of cobalt deficiency on synthetic rations in which the cobalt concentrations have been reduced well below those which will induce symptoms of cobalt deficiency in ruminants. Houk et al. have shown this for rats on a ration claimed to contain only 0.003 p.p.m. Co, and Thompson and Ellis ° for rabbits on a ration claimed to contain only 0.0024 p.p.m. Co. It is apparent that if these species require cobalt at all it must be in extraordinarily small amounts. 

Fig. 1. Typical responses of ewes on cobalt>deficient pastures. R53, untreated R57,1 mg. Co daily per os R60,1 mg. Co daily injected R50,1 mg. Co daily injected plus 1 mg. Co daily injected after 50 weeks when the deficiency symptoms were in a terminal stage. S denotes recognizable deficiency systems. (Marston and Lee. )...

DEFICIENCY SYMPTOMS. A cobalt deficiency as such has never been produced in humans. The signs and symptoms that are sometimes attributed to cobalt deficiency are actually due to lack of vitamin B-12, characterized by pernicious anemia, poor growth, and occasionally neurological disorders. 

Symptoms of chronic cobalt toxicity in humans occurred in anemic persons undergoing therapy with iron supplements to which cobalt was added to promote iron absorption and to stimulate erythropoiesis. Depending on the degree of iron deficiency and the amount of iron supplement prescribed, patients thus treated could typically receive from 0.17 to 3.19 mg Co kg per day over periods of days to many months. 

B. Chronic toxicity to the hematologic and nervous systems results from inactivation of vitamin following irreversible oxidation of its cobalt atom. Vitamin Bi2 is required for the synthesis of methionine, which is essential for DNA synthesis and maintenance of myelin. Use of nitrous oxide can precipitate neurological symptoms in patients with subclinical B,2 or folic acid deficiency. 

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