User:Gzorg/Vitamin B12 20160522

Main article : Vitamin B12

= Table =

= Facts from Vitamin B12 article =


 * 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 &quot;debatable&quot;
 * 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 =

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

= Little story =

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
 * 2) * Haptocorrin is produced
 * 3) * Some cobalamin binds to Haptocorrin
 * 4) Stomach
 * 5) * Free cobalamin is attacked by stomach acids
 * 6) * Bound cobalamin is protected from the stomach acids
 * 7) * Intrinsic factor is produced
 * 8) Duodenum
 * 9) * Panceratic protease frees the bound cobalamin
 * 10) * Free cobalamin binds to the intrinsic factor
 * 11) Epithelial cell
 * 12) * Only cobalamin bound to intrinsic factor can enter the epithelial cells
 * 13) * Inside the cell, cobalamin is freed again
 * 14) * Transcobalamin II binds to the three cobalamin
 * 15) * Only cobalamin bound to transcobalamin II can exit the epithelial cells

= See also ==


 * Vitamin B12
 * Hydroxocobalamin
 * Cyanocobalamin
 * Methylcobalamin
 * Cobamamide
 * Haptocorrin
 * Transcobalamin
 * Intrinsic factor