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Structural formula
Structure of cholecalciferol
Common name Vitamin D 3
other names
  • Colecalciferol ( INN )
  • Calciol
  • (3 β , 5 Z , 7 E ) -9,10-secocholesta- 5,7,10 (19) -trien-3-ol
  • 3- [2- [7a-methyl-1- (6-methylheptan-2-yl) - 2,3,3a, 5,6,7-hexahydro- 1 H -inden-4-ylidene] ethylidene] -4- methylidene-cyclohexan-1-ol
Molecular formula C 27 H 44 O
CAS number 67-97-0
PubChem 5280795
ATC code

A11 CC05

DrugBank DB00169
Brief description colorless solid
Occurrence non-vegetable eukaryotes
function Precursor of calcitriol , as such: regulation of the calcium balance, maturation of immune cells
Daily need 20 µg (800 IU ) daily (sum of skin production and food intake)
Consequences in case of deficiency Rickets , osteomalacia
Overdose See hypervitaminosis D.
Molar mass 384.64 g mol −1
Physical state firmly
Melting point

84-85 ° C

boiling point


solubility fat-soluble, 50-80% protein-bound in the blood (to VDBP )
safety instructions
Please note the restricted labeling requirements for drugs, medical devices, cosmetics, food and animal feed
GHS hazard labeling from  Regulation (EC) No. 1272/2008 (CLP) , expanded if necessary
06 - Toxic or very toxic 08 - Dangerous to health


H and P phrases H: 330-311-301-372
P: 280-304 + 340-302 + 352-309 + 310
Toxicological data

42 mg kg −1 ( LD 50ratoral )

As far as possible and customary, SI units are used. Unless otherwise noted, the data given apply to standard conditions .

Cholecalciferol (also cholecalciferol or shortly CALCIOL ; vitamin D 3 or inaccurate vitamin D ) is the main physiological form of vitamin D in all non-plant eukaryotes and so also in humans. Cholecalciferol is a secosteroid and is also formed in the body with the help of UVB radiation (Dorno radiation, according to Carl Dorno ) in the skin from 7-dehydrocholesterol , which is why the historical term vitamin is not entirely accurate by definition.

It is found in food mainly in fatty fish or is added to food as a dietary supplement . It has the function of a prohormone in the body and is converted into its physiologically effective form, the hormone calcitriol , via the intermediate calcidiol .

Cholecalciferol can from the offal bovine brain are made.


Cholecalciferol plays an essential role in regulating the calcium level in the blood and in building bones.

Biosynthesis of vitamin D 3

Most vertebrates, including humans, get much of their vitamin D needs from sun exposure of their skin; this also occurs with certain types of plankton (phytoplankton coccolithophor Emeliani huxleii ).

By definition, vitamins are substances that the body cannot produce itself, but which are required for life and must therefore be supplied. The precursors of the so-called vitamin D 3 are produced by the body itself. In addition to the provitamin 7-dehydrocholesterol present in the body (the starting substance for vitamin D synthesis), sunlight must then be added. Vitamin D 3 is therefore known as a vitamin for historical reasons. Due to its endogenous synthesis and the fact that its effect affects other tissues in addition to the site of synthesis, vitamin D 3 should be called a prohormone .

If 7-dehydrocholesterol is irradiated with ultraviolet with wavelengths in the range 290-315 nm (UV-B radiation) and at least 18 mJ / cm², the B-ring in 7-dehydrocholesterol can be broken up by a photochemically induced 6-electron conrotatory electrocyclic reaction : Previtamin D 3 is produced . Previtamin D 3 is thermodynamically unstable and is subject to a (1-7) sigmatropic rearrangement in which a proton migrates from C-19 to C-9, with subsequent isomerization: Vitamin D 3 is formed . Vitamin D 3 gets into the blood and is mainly bound to the vitamin D binding protein (DBP) transported to the liver, where it is further hydroxylated to calcidiol (25 (OH) -vitamin D 3 ). In the test tube, 80% of the previtamin D 3 is isomerized to vitamin D 3 after three days , in the skin this happened after eight hours.

Self-regulation of ultraviolet-induced synthesis

If 7-dehydrocholesterol is exposed to simulated equatorial solar radiation in a test tube experiment, approx. 20% of the initial amount is converted to previtamin D 3 after a few minutes . This amount of previtamin D 3 remains in equilibrium with further irradiation, because previtamin D 3 is also photolabile and is broken down into physiologically inactive lumisterol and tachysterol over the next eight hours by further UV-B irradiation , before it isomerizes to vitamin D 3 . During this time, the 7-dehydrocholesterol drops to about 30% of the initial amount. On the other hand, under unnatural narrow-spectrum UV-B irradiation with a wavelength of 290 to 300 nm, 65% of the original 7-dehydrocholesterol is converted into previtamin D 3 .

The vitamin D 3 produced from previtamin D 3 is also photolabile: If vitamin D 3 cannot be removed quickly enough in the blood, UV-B and UV-A radiation (up to 345 nm) produce at least three more ineffective ones Products: Suprasterol-1 and -2 and 5,6-Transvitamin D 3 .

Short exposure to sunlight (with a sufficiently high UV-B component) produces a similar amount of vitamin D 3 for a few minutes as a comparable exposure over a longer period of time. As a result, the body is briefly protected from vitamin D intoxication caused by too much radiation.

In the long term, there is protection against vitamin D intoxication through increased formation of melanin ( tanning , darker skin type in southern countries) in the skin, which absorbs ultraviolet at wavelengths 290-320 nm.

The 7-dehydrocholesterol content of the skin decreases with age. In addition, the ability of the skin to produce vitamin D 3 decreases with age by a factor of approximately 3 compared to a 20-year-old person.

For the pale skin of a fair-skinned young adult, the minimum erythema dose (MED) (when the skin starts to turn red) is reached after 10 to 12 minutes on a sunny summer afternoon at 42 ° latitude at sea level (corresponding to Boston, Barcelona or Rome) , a dark-skinned person needs 120 minutes. If the whole body of these people's skin is irradiated, it releases an amount comparable to 10,000 to 20,000 IU (250 µg to 500 µg) of vitamin D 3 from food into the blood within the next 24 hours  , a multiple of the recommended diet of 200 to 500 IU of vitamin D 3 daily. A strong formation of vitamin D 3 in the skin is therefore possible even with short but intense exposure to sunlight with a high UV-B content.

Since the bone density in dark-skinned people is not reduced by the somewhat reduced vitamin D formation due to the lower permeability of the skin to UV rays, it is assumed that dark-skinned people have a lower concentration of the vitamin D-binding protein.


Vitamin D 3
25-hydroxylation of vitamin D 3

Vitamin D 3 , mainly bound to the vitamin D-binding protein , is transported to the liver via the blood. There it is hydroxylated by the enzyme cytochrome P450 2R1 in the microsomes to calcidiol (25 (OH) -Vitamin-D 3 ). An earlier assumption that this reaction also takes place in the mitochondria has now been refuted.

Calcidiol (25 (OH) -Vitamin-D 3 ) is bound to vitamin D-binding protein again in the liver and released into the blood. There it has a half-life of approx. 19 days.

This enzymatic reaction is probably not subject to any regulation worth mentioning, since the 25 (OH) vitamin D 3 level in the blood pretty much reflects the longer-term vitamin D 3 supply of the last three to four months, while the vitamin D 3 level shows the supply of the last hours to days.

Conversion into vitamin D.

Calcidiol (25 (OH) -Vitamin-D 3 ) is a storage form of vitamin D 3 . There has to be one in order to be able to intercept the large peaks and pauses in the main vitamin D supply through light. The medium to long-term vitamin D supply of an organism can best be determined via the blood level of the calcidiol (see below for details).

Breakdown of vitamin D 3

1,25 (OH) 2 D 3 (calcitriol) is broken down by 24-hydroxylase to water-soluble calcitroic acid , which is excreted in the bile . The 24-hydroxylase is encoded by the gene CYP24A1.

Vitamin D deficiency

See also: Vitamin D3 deficiency

A vitamin D deficiency leads in the medium term to rickets in children and osteomalacia in adults . A vitamin D deficiency has adverse effects on the following diseases:

Natural sources

Food intake usually only covers 5 to 20% of the vitamin D 3 requirement. Direct exposure of the skin to sunlight is therefore essential for vitamin D 3 formation. On sunny summer days, this alone covers the daily requirement many times over. In the winter months, however, formation through exposure to the sun is not possible because of the lack of UV-B in sunlight. The vitamin D reserves built up in the body in summer and food are then the only natural sources.

Education through sunlight

The UV-B component in sunlight is responsible for the formation of vitamin D 3 through exposure to the sun. Various factors influence the light intensity and the final vitamin D 3 formation in the skin, such as: B. the skin color of the person, the position of the sun, the height above sea level, the nature of the earth's surface, the clouds, smog or the ozone . Window glass absorbs almost all UV-B components in sunlight and sunscreen prevents vitamin D 3 production by more than 97% even at SPF 8. A visit to the solarium is usually not beneficial, as the skin is usually irradiated with UV-A and not with UV-B light.

Absorption through food

Vitamin D 3 is not a common food component. The recommended daily requirement ( RDA ) of vitamin D 3 is being discussed among scientists and those responsible for health care. Current recommendations are considered by researchers in the field to be either irrelevant (for people sufficiently exposed to UV-B light) or inadequate (for the majority of the higher latitude population). For groups at risk of vitamin D deficiency (darker skin color, lack of light and other causes), a check of the vitamin D level is recommended. A daily oral dose of 400 international units (IU) is recommended for children in the first year of life . A daily oral intake of 600 IU is recommended for pregnant and breastfeeding women.

Vitamin D determination

The determination of the vitamin D level in the blood serum only reflects the vitamin D uptake with food or the self-synthesis in the skin during the last hours or days. For an investigation of the long-term vitamin D status , it makes more sense to determine the calcidiol level in the blood, into which vitamin D 3 is quickly converted in the liver (see above). The half-life of calcidiol in the blood circulation is 1–2 months, depending on the overall vitamin D status. It takes up to four months until a new steady state with a stable serum value is established after a change in the daily vitamin D intake.

The calcidiol can be determined since the beginning of the 1980s and enabled a further understanding of the physiology of vitamin D 3 . The measured values ​​are given either in weight or molar concentration units, with 1 ng / ml corresponding to around 2.5 nmol / l.

Overdose and toxicity

Acute or chronic vitamin D overdose can lead to vitamin D hypervitaminosis. In 2012, the European Food Safety Authority (EFSA) issued the following statement on the safety of vitamin D 3 :

A maximum daily dose of 100 µg (4000 IU) for adolescents and adults (including pregnant women and nursing mothers) and 50 µg (2000 IU) for children from 1 to 10 years of age can be taken long-term by healthy people without the risk of side effects, even without medical supervision.
Measured against the usual vitamin D doses, this statement even allows more leeway for adults: The EFSA cites 2 studies that established a NOAEL (no observed adverse effect level) for vitamin D of 250 µg (10,000 IU). The safety range is less for infants.

Most authors consider a daily intake of up to 100 µg (4000 IU) of vitamin D 3 for adults for six months as safe, i.e. without any verifiable side effects such as increased calcium excretion in the urine.

The package inserts for pharmacy-only vitamin D preparations indicate an overdose threshold of between 40,000 and 100,000 IU per day for 1 to 2 months for adults with normal function of the parathyroid glands. Infants and small children can be sensitive to much lower doses. The leaflet for a drug is usually considered to be both medically and legally decisive.

Use to control rodents

Cholecalciferol can also be used as a rat poison or poison against rodents : the LD 50 (oral) in rats is around 42 mg / kg body weight, in house mice around 43 mg / kg body weight and in the small bandicota rat ( Bandicota bengalensis ) depending on gender at 31-35 mg / kg. Since cholecalciferol seldom occurs freely in nature, rodents could not develop an evolutionary tolerance towards high doses. Originally it was assumed that, as a rodenticide , it was weakly toxic to other species, such as dogs or cats ; but it turned out that this is not the case. For dogs, an LD 50 of approx. 88 mg / kg body weight applies , deaths have already occurred at 2 mg / kg, puppies in particular are more susceptible. Cats are more resistant. In New Zealand , baits containing cholecalciferol have been used successfully in field trials to combat the fox kusu .

Cholecalciferol is approved in the EU and Switzerland for use as a biocide of product type 14 ( rodenticides ).

Trade names

Monopreparations : Dekristol (D), Vigantol (D), Oleovit D3 (A), various food supplements

See also


Web links

Wikibooks: Vitamin D Metabolism  - Learning and Teaching Materials
Wikibooks: Bile Acid Metabolism  - Learning and Teaching Materials

Individual evidence

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