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Cobalt poisoning is intoxication caused by excessive levels of cobalt in the body. Cobalt is an essential element for health in animals in minute amounts as a component of vitamin B 12. A deficiency of cobalt, which is very rare, is also potentially lethal, leading to pernicious anemia. [1]
Vitamin B 12 deficiency is preventable with supplements, which are recommended for pregnant vegetarians and vegans, and not harmful in others. [2] Risk of toxicity due to vitamin B 12 is low. [2] Vitamin B 12 deficiency in the US and the UK is estimated to occur in about 6 percent of those under the age of 60, and 20 percent of those over the ...
Cobalt is essential to the metabolism of all animals. It is a key constituent of cobalamin, also known as vitamin B 12, the primary biological reservoir of cobalt as an ultratrace element. [1] [2] Bacteria in the stomachs of ruminant animals convert cobalt salts into vitamin B 12, a compound which can only be produced by bacteria or archaea.
Common, most foods do not contain vitamin D, indicating that a deficiency will occur unless people get sunlight exposure or eat manufactured foods purposely fortified with vitamin D. Vitamin D deficiency is a known cause of rickets, and has been linked to numerous other health problems. [46] [47] Vitamin E deficiency
[6] [15] [26] Vitamin B 12 deficiency can also cause symptoms of mania and psychosis. [27] [28] Among other problems, weakened immunity, reduced fertility and interruption of blood circulation in women may occur. [29] The main type of vitamin B12 deficiency anemia is pernicious anemia, [30] characterized by a triad of symptoms:
[4]: 44 Vitamin B 12 is an essential water-soluble vitamin, the deficiency of which creates anemia (macrocytic anemia), decreased bone marrow cell production (anemia, pancytopenia), neurological problems, as well as metabolic issues (methylmalonyl-CoA acidosis). [4]: 50–51 Vitamin B 12 is therefore an important vitamin for the body to absorb.
The enzyme is bound to adenosylcobalamin, a hormonal derivative of vitamin B12 in order to function. Methylmalonyl-CoA mutase deficiency [2] is caused by genetic defect in the MUT [3] gene responsible for encoding the enzyme. Deficiency in this enzyme accounts for 60% of the cases of methylmalonic acidemia. [4]
In molecular biology, the vitamin B12-binding domain is a protein domain which binds to cobalamin (vitamin B12). It can bind two different forms of the cobalamin cofactor, with cobalt bonded either to a methyl group (methylcobalamin) or to 5'-deoxyadenosine (adenosylcobalamin).