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User:Gzorg/Vitamin B12 20160522

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Main article : Vitamin B12

Table

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Vitamer Picture
Cyanocobalamin
Hydroxocobalamin
Methylcobalamin
Adenosylcobalamin
Dibencozide
Cobamamide

Facts from Vitamin B12 article

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  • Main vitamer is cobalamin
  • Cobalamin is water-solube
  • Key roles:
    • nervous system
    • formation of red blood cells
    • DNA synthesis
    • fatty acid metabolism
    • amino acid metabolism
  • Fungi, plants, and animals can't produce it. Only some bacteria and archaea have the enzymes needed for its synthesis.
  • Plants that are source of vitamin B12 get it from bacterial symbiosis.
  • Industrial production requires a bacterial fermentation-synthesis.
  • Synthetic vitamin B12 is a form that has been produced using such a process.
  • All vitamin B12 vitamers show pharmacological activity.
  • Cobalt
    • Vitamin B12 contains cobalt, which is a rare element.
    • The tetra-pyrrole ring containg the cobalt is a called the corrin ring.
  • Bacterial hydroxocobalamin
    • Bacteria produces hydroxocobalamin.
    • Conversion of hydroxocobalamin into other forms occurs in the human body.
  • Cyanocobalamin
    • Cyanocobalamin is produced by modifying bacterial hydroxocobalamin.
    • Cyanocobalamin is mareketed instead of hydroxocobalamin because of superior stability.
    • In the body, cyanocobalamin is converted to methylcobalamin and 5'-deoxyadenosylcobalamin.
    • Conversion of cyanocobalamin to methylcobalamin and 5'-deoxyadenosylcobalamin leave a cyanide ion.
    • Cyanide ions are bad for the human body, but less cyanide is produced than cyanide that comes from food.
    • 20 µg of cyanide is produced per 1,000 µg of cyanocobalamin.
    • The other vitamers (hydroxocabalamin, methylcobalamin, and adenosylcobalamin) are cyanide-free.
    • Superiority of the cyanid-free vitamers to cyanocobalamin is "debatable"
  • Pernicious anemia and other causes of vitamin B12 deficiency
    • Pernicious anemia is an autoimmune disease in which parietal cells of the stomach are destroyed.
    • Without such cells, some (intrinsic factor)(?) and and digestive acids are not produced.
    • (Intrinsic factor)(?) is crucial for the normal absorption of vitamin B12.
    • Lack of that (Intrinsic factor)(?) causes vitamin B12 deficiency.
    • There are other subtler kinds of vitamin B12 deficiency whose effects have been elucidated.
  • Pseudovitamin-B12
    • Pseudovitamin-B12 vitamer analogues that are biologically inactive in humans
    • They are found to be present alongside active vitamers in humans, in many food sources and possibly in supplements and fortified foods.
    • They are found to predominate in most cyanobacteria and in some algae.
    • Examples include Spirulina and dried Asakusa-nori (Porphyra tenera).
  • Medical uses
    • Vitamin B12 is used to treat vitamin B12 deficiency
    • Vitamin B12 is used to treat cyanide poisoning
      • Hydroxocobalamin, possibly with sodium thiosulfate, induce cyanide ions to take the place of the hydroxide ligand
      • This leads to the harmless cyanocobalamin which is then excreted in urine
      • That treatment was FDA-approved in 2006
      • This is the reverse of the usual process of converting cyancobolamin into hydroxocobalamin.
      • This shows that conversion from cyancobolamin to hydroxocobalamin or from hydroxocobalamin to cyancobolamin is a statistical process in the body
      • Lots of hydroxocobalamin + lots of cyanide => some cyanocobolamin and some less cyanide
      • Lots of cyanocobolamin => some more cyanide and some hydroxocobalamin
      • Some conditions may influence one way of the reaction or the other.
    • Vitamin B12 is used to hereditary deficiency of transcobalamin II
    • Vitamin B12 is given as part of the Shilling test for detecting pernicious anemia.
    • High vitamin B12 levels in elderly individuals may protect against
      • brain atrophy
      • shrinkage associated with Alzheimer's disease
      • impaired cognitive function

Facts from Hydroxycobalamin article

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  • Color
    • Most Vitamin B12 vitamers have an intense red color
  • Conversion
    • In humans, hydroxycobalamin is rapidly converted to usable coenzyme forms of Vitamin B12
  • Uses
    • vitamin B12 deficiency
    • cyanide poisoning
    • scavenger of nitric oxide
  • DNA synthesis
    • cobalamins are essential cofactors required for DNA synthesis
    • DNA synthesis occurs notably in bone marrow and myeloid cells
  • reactions
    • mitochondrial methylmalonyl-CoA mutase conversion of methylmalonic acid to succinate
      • links lipid and carbohydrate metabolism
    • activation of methionine synthase
      • rate-limiting step in the synthesis of methionine from homocysteine and 5-methyltetrahydrofolate
  • WHO
    • Hydroxycobalamin (or cobalamins as a group) is on the WHO Model List of Essential Medicines
  • Deficiency
    • Vitamin B12 defiency can be treated by intramuscular injection of either hydroxycobalamin or cyanocobalamin
    • Cyanocobalamin is traditionally prescribed in the United States.
    • Outside of the United States, hydroxocobalamin is preferred
    • Hydroxocobalamin is considered the “drug of choice” for vitamin B12 deficiency by the Martindale Extra Pharmacopoeia and the WHO Model List of Essential Drugs.
    • Hydroxocobalamin has a longer retention in the body
    • Hydroxocobalamin requires less-frequent IM injections for restoring vitamin B12 serum levels
    • IM administration of hydroxocobalamin is the preferred treatment for
      • pediatric patients with intrinsic cobalamin metabolic diseases
      • vitamin B12-deficient patients with tobacco amblyopia due to cyanide poisoning
      • patients with pernicious anemia who have optic neuropathy
  • Levels
    • Defiency is recognized when serum levels are less than 200 pg/ml
    • Daily IM injections of hydroxocobalamin up to 1 mg per day are then prescribed
    • if neurological symptoms persist, injections up to weekly or biweekly are recommended for six months
    • then monthly IM injections are considered sufficient
    • after clinical improvement is confirmed, maintenance supplementation will generally be needed for life
  • Properties
    • Hydroxocobalamin acetate
      • odorless
      • dark-red
      • orthorhombic needles
    • injection formulations
      • clear
      • dark-red
    • distribution coefficient: 1.133 × 10-5
    • pKa : 7.65
  • Causes of deficiency
    • Dietary deficiency
    • Malabsorption
    • damage to the stomach where intrinsic factor is secreted
    • damage to the ileum where intrinsic factor facilitates vitamin B12 absorption
      • tropical sprue and nontropical sprue
    • Inadequate secretion of intrinsic factor
      • lesions that destroy the gastric mucosa
        • ingestion of corrosives
        • extensive tumors
        • conditions associated with gastric atrophy
          • multiple sclerosis
          • endocrine disorders
          • iron deficiency
          • subtotal gastrectomy
      • Structural lesions
        • regional ileitis
        • ileal reactions
        • malignancies
    • Competition for vitamin B12 by intestinal parasites or bacteria
      • Diphyllobothrium latum
    • blind loop syndrome

Inadequate use of vitamin B12, which may occur if antimetabolites for the vitamin are employed in the treatment of neoplasia

Little story

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Characters:

  • Cobalamin : any of the B12 vitamers
  • Haptocorrin, aka. cobalophilin, transcobalamin-1, TC-1, transcobalamin I, TCN1, R-factor, R-protein
  • Intrinsic factor, aka. IF, gastro intrinsic factor, GIF
  • Transcobalamin-2, aka. transcobalamin II, TCN2

Play:

  1. Mouth
    • Haptocorrin is produced
    • Some cobalamin binds to Haptocorrin
  2. Stomach
    • Free cobalamin is attacked by stomach acids
    • Bound cobalamin is protected from the stomach acids
    • Intrinsic factor is produced
  3. Duodenum
    • Panceratic protease frees the bound cobalamin
    • Free cobalamin binds to the intrinsic factor
  4. Epithelial cell
    • Only cobalamin bound to intrinsic factor can enter the epithelial cells
    • Inside the cell, cobalamin is freed again
    • Transcobalamin II binds to the three cobalamin
    • Only cobalamin bound to transcobalamin II can exit the epithelial cells

See also =

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