Main article : Vitamin B12
Table edit
| Vitamer | Picture |
|---|---|
| Cyanocobalamin | 
|
| Hydroxocobalamin | 
|
| Methylcobalamin | 
|
| Adenosylcobalamin | 
|
| Dibencozide | |
| Cobamamide |
Facts from Vitamin B12 article edit
- 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 edit
- 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
- mitochondrial methylmalonyl-CoA mutase conversion of methylmalonic acid to succinate
- 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
- Hydroxocobalamin acetate
- 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
- lesions that destroy the gastric mucosa
- 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 edit
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:
- Mouth
- Haptocorrin is produced
- Some cobalamin binds to Haptocorrin
- Stomach
- Free cobalamin is attacked by stomach acids
- Bound cobalamin is protected from the stomach acids
- Intrinsic factor is produced
- Duodenum
- Panceratic protease frees the bound cobalamin
- Free cobalamin binds to the intrinsic factor
- 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