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Cholecalciferol

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Cholecalciferol
INN:Colecalciferol
Clinical data
Pronunciation/ˌkoʊləkælˈsɪfərɒl/
Other namesvitamin D3,calciol, activated 7-dehydrocholesterol
AHFS/Drugs.comProfessional Drug Facts
License data
Routes of
administration		By mouth,intramuscular
ATC code
Legal status
Legal status
Identifiers
  • (3S,5Z,7E)-9,10-secocholesta-5,7,10(19)-trien-3-ol
CAS Number
PubChemCID
DrugBank
ChemSpider
UNII
KEGG
ChEBI
ChEMBL
CompTox Dashboard(EPA)
ECHA InfoCard100.000.612Edit this at Wikidata
Chemical and physical data
FormulaC27H44O
Molar mass384.648g·mol−1
3D model (JSmol)
Melting point83 to 86 °C (181 to 187 °F)
Boiling point496.4 °C (925.5 °F)
Solubility in waterPractically insoluble in water, freely soluble in ethanol, methanol and some other organic solvents. Slightly soluble in vegetable oils.
  • O[C@@H]1CC(\C(=C)CC1)=C\C=C2/CCC[C@]3([C@H]2CC[C@@H]3[C@H](C)CCCC(C)C)C
  • InChI=1S/C27H44O/c1-19(2)8-6-9-21(4)25-15-16-26-22(10-7-17-27(25,26)5)12-13-23-18-24(28)14-11-20(23)3/h12-13,19,21,24-26,28H,3,6-11,14-18H2,1-2,4-5H3/b22-12+,23-13-/t21-,24+,25-,26+,27-/m1/s1☒N
  • Key:QYSXJUFSXHHAJI-YRZJJWOYSA-N

Cholecalciferol,also known asvitamin D3andcolecalciferol,is a type ofvitamin Dthat is made by the skin when exposed to UV-B light; it is found in some foods and can be taken as adietary supplement.[3]

Cholecalciferol is made in the skin followingUVB lightexposure.[4]It is converted in the liver tocalcifediol(25-hydroxyvitamin D) which is then converted in the kidney tocalcitriol(1,25-dihydroxyvitamin D).[4]One of its actions is to increasecalciumuptake by the intestines.[5]It is found in food such as somefish,beef liver, eggs, and cheese.[6][7]Plants, cow milk, fruit juice, yogurt, and margarine also may have cholecalciferol added to them in some countries, including the United States.[6][7]

Cholecalciferol can be taken as an oral dietary supplement to preventvitamin D deficiencyor as a medication to treat associated diseases, includingrickets.[8][9]It is also used forfamilial hypophosphatemia,hypoparathyroidismthat is causinglow blood calcium,andFanconi syndrome.[9][10]Vitamin-D supplements may not be effective in people with severekidney disease.[11][10]Excessive doses in humans can result in vomiting, constipation, weakness, and confusion.[5]Other risks includekidney stones.[11]Doses greater than40000IU(1000 μg) per day are generally required beforehigh blood calciumoccurs.[12]Normal doses,800–2000IU per day, are safe inpregnancy.[5]

Cholecalciferol was first described in 1936.[13]It is on theWorld Health Organization's List of Essential Medicines.[14]In 2021, it was the 65th most commonly prescribed medication in the United States, with more than 10million prescriptions.[15][16]Cholecalciferol is available as ageneric medicationandover the counter.[10][17][18]

Medical uses[edit]

Cholecalciferol (vitamin D3) appears to stimulate the body'sinterferon type Isignaling system that protects against bacteria and viruses, unlikevitamin D2.[19]

For psoriasis, cream that includes vitamin D3 can have a good effect, or UVB phototherapy.

Vitamin D deficiency[edit]

Main article:Vitamin D deficiency

Cholecalciferol is a form of vitamin D which is naturally synthesized in skin and functions as a pro-hormone, being converted tocalcitriol.This is important for maintaining calcium levels and promoting bone health and development.[4]As a medication, cholecalciferol may be taken as a dietary supplement to prevent or to treat vitamin D deficiency. One gram is40000000(40×106)IU,equivalently1 IUis0.025 μg,or25 ng.Dietary reference intake values for vitamin D (ergocalciferol,which is D2,or cholecalciferol, which is D3), or both, have been established and recommendations vary depending on the country:

  • In the US:15 μg/d(600 IU/d) for all individuals (males, females, pregnant/lactating women) between the ages of 1 and 70 years, inclusive. For all individuals older than 70 years,20 μg/d(800 IU/d) is recommended.[20]
  • In the EU:15 μg/d(600 IU/d) for all people older than 1 year and10 μg/d(400 IU/d) for infants aged 7–11 months, assuming minimal cutaneous vitamin D synthesis.[21]
  • In the UK: a ‘Safe Intake’ (SI) of8.5–10 μg/d(30–400 IU/d) for infants < 1 year (including exclusively breastfed infants) and an SI of10 μg/d(400 IU/d) for children aged 1 to <4 years; for all other population groups aged 4 years and more (including pregnant/lactating women) a Reference Nutrient Intake (RNI) ofday10 μg(400 IU/d).[22]

Low levels of vitamin D3 are more commonly found in individuals living in northern latitudes or with other reasons for a lack of regular sun exposure, including being housebound, frail, elderly, or obese, having darker skin, and wearing clothes that cover most of the skin.[23][24]Supplements are recommended for these groups of people.[24]

TheInstitute of Medicinein 2010 recommended a maximum uptake of vitamin D of4000 IU/d,finding that the dose for lowest observed adverse effect level is 40,000 IU daily for at least 12 weeks,[25]and that there was a single case of toxicity above10000IUafter more than seven years of daily intake; this case of toxicity occurred in circumstances that have led other researchers to dispute whether it is a credible case to consider when making vitamin D intake recommendations.[25]Patients with severe vitamin D deficiency will require treatment with aloading dose;its magnitude can be calculated based on the actual serum 25-hydroxy-vitamin D level and body weight.[26]

There are conflicting reports concerning the relative effectiveness of cholecalciferol (D3) versusergocalciferol(D2), with some studies suggesting less efficacy of D2,and others showing no difference. There are differences in absorption, binding and inactivation of the two forms, with evidence usually favoring cholecalciferol in raising levels in blood, although more research is needed.[27]

A much less common use of cholecalciferol therapy inricketsutilizes a single large dose and has been calledstosstherapy.[28][29][30]Treatment is given either orally or byintramuscular injectionof300000IU(7500 μg) to500000IU(12500μg=12.5 mg), in a single dose, or sometimes in two to four divided doses. There are concerns about the safety of such large doses.[30]

Low circulating vitamin D levels have been associated with lower totaltestosteronelevels in males. Vitamin D supplementation could potentially improvetotal testosterone concentration,although more research is needed.[31]

Other diseases[edit]

A meta-analysis of 2007 concluded that daily intake of1000 to 2000 IU/dof vitamin D3could reduce the incidence of colorectal cancer with minimal risk.[32]Also a 2008 study published in Cancer Research has shown the addition of vitamin D3(along with calcium) to the diet of some mice fed a regimen similar in nutritional content to a new Western diet with 1000 IU cholecalciferol per day prevented colon cancer development.[33]In humans, with400 IUdaily, there was no effect of cholecalciferol supplements on the risk of colorectal cancer.[34]

Supplements are not recommended for prevention of cancer as any effects of cholecalciferol are very small.[35]Although correlations exist between low levels of blood serum cholecalciferol and higher rates of various cancers,multiple sclerosis,tuberculosis,heart disease, and diabetes,[36]the consensus is that supplementing levels is not beneficial.[37]It is thought that tuberculosis may result in lower levels.[38]It, however, is not entirely clear how the two are related.[39]

Biochemistry[edit]

Structure[edit]

Cholecalciferol is one of the five forms ofvitamin D.[40]Cholecalciferol is asecosteroid,that is, a steroid molecule with one ring open.[41]

Mechanism of action[edit]

By itself cholecalciferol is inactive. It is converted to its active form by twohydroxylations:the first in the liver, byCYP2R1orCYP27A1,to form 25-hydroxycholecalciferol (calcifediol,25-OH vitamin D3). The second hydroxylation occurs mainly in the kidney through the action ofCYP27B1to convert 25-OH vitamin D3into 1,25-dihydroxycholecalciferol (calcitriol,1,25-(OH)2vitamin D3). All these metabolites are bound in blood to thevitamin D-binding protein.The action of calcitriol is mediated by thevitamin D receptor,anuclear receptorwhich regulates the synthesis of hundreds of proteins and is present in virtually every cell in the body.[4]

Biosynthesis[edit]

Click on icon in lower right corner to open.

Click on genes, proteins and metabolites below to link to respective articles.[§ 1]

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|alt=Vitamin D Synthesis Pathway (view/edit)]]
Vitamin D Synthesis Pathway (view/edit)
  1. ^The interactive pathway map can be edited at WikiPathways:"VitaminDSynthesis_WP1531".

7-Dehydrocholesterolis the precursor of cholecalciferol.[4]Within the epidermal layer of skin, 7-dehydrocholesterol undergoes anelectrocyclic reactionas a result ofUVB lightatwavelengthsbetween290 and 310 nm,with peak synthesis occurring at293 nm.[42]This results in the opening of the vitamin precursor B-ring through aconrotatorypathway makingprevitamin D3(pre-cholecalciferol).[43]In a process which is independent of UV light, the pre-cholecalciferol then undergoes a [1,7] antarafacialsigmatropicrearrangement[44]and therein finally isomerizes to form vitamin D3.

The active UVB wavelengths are little present in sunlight, and sufficient amounts of cholecalciferol can be produced with moderate exposure of the skin, depending on the strength of the sun.[42]Time of day, season, latitude, and altitude affect the strength of the sun, and pollution, cloud cover or glass all reduce the amount of UVB exposure. Exposure of face, arms and legs, averaging5–30minutes twice per week, may be sufficient, but the darker the skin, and the weaker the sunlight, the more minutes of exposure are needed. Vitamin D overdose is impossible from UV exposure; the skin reaches an equilibrium where the vitamin degrades as fast as it is created.[42]

Cholecalciferol can be produced in skin from the light emitted by the UV lamps intanning beds,which produce ultraviolet primarily in theUVAspectrum, but typically produce 4% to 10% of the total UV emissions as UVB. Levels in blood are higher in frequent users of tanning salons.[42]

A 293 nanometer UVB light emitting diode (LED) was found to be 2.4 times more efficient in producing vitamin D3 than the sun in less than1⁄60the time. (https://pubmed.ncbi.nlm.nih.gov/28904394/).

Whether cholecalciferol and all forms of vitamin D are by definition "vitamins"can be disputed, since the definition of vitamins includes that the substance cannot be synthesized by the body and must be ingested. Cholecalciferolissynthesized by the body during UVB radiation exposure.[4]

The three steps in the synthesis and activation of vitamin D3are regulated as follows:

  • Cholecalciferol is synthesized in the skin from 7-dehydrocholesterol under the action of ultraviolet B (UVB) light. It reaches an equilibrium after several minutes depending on the intensity of the UVB in the sunlight – determined by latitude, season, cloud cover, and altitude – and the age and degree of pigmentation of the skin.
  • Hydroxylation in the endoplasmic reticulum of liverhepatocytesof cholecalciferol to calcifediol (25-hydroxycholecalciferol) by25-hydroxylaseis loosely regulated, if at all, and blood levels of this molecule largely reflect the amount of cholecalciferol produced in the skin combined with any vitamin D2or D3ingested.
  • Hydroxylation in the kidneys of calcifediol to calcitriol by1-alpha-hydroxylaseis tightly regulated: it is stimulated byparathyroid hormoneand serves as the major control point in the production of the active circulating hormonecalcitriol(1,25-dihydroxyvitamin D3).[4]

Industrial production[edit]

Cholecalciferol is produced industrially for use invitamin supplementsandto fortify foods.As apharmaceutical drugit is called cholecalciferol (USAN) or colecalciferol (INN,BAN). It is produced by theultravioletirradiation of7-dehydrocholesterolextracted fromlanolinfound in sheep'swool.[45]Cholesterol is extracted from wool grease and wool wax alcohols obtained from the cleaning of wool after shearing. The cholesterol undergoes a four-step process to make 7-dehydrocholesterol, the same compound that is produced in the skin of animals. The 7-dehydrocholesterol is then irradiated with ultraviolet light. Some unwantedisomersare formed during irradiation: these are removed by various techniques, leaving a resin which melts at about room temperature and usually has a potency of25000000to 30000000International Units/gram.

Cholecalciferol is also produced industrially for use in vitamin supplements fromlichens,which is suitable for vegans.[46][47]

Stability[edit]

Cholecalciferol is very sensitive toUV radiationand will rapidly, but reversibly, break down to form supra-sterols, which can further irreversibly convert toergosterol.[citation needed]

Pesticide[edit]

Rodents are somewhat more susceptible to high doses than other species, and cholecalciferol has been used in poison bait for the control of these pests.[48][18]

The mechanism of high dose cholecalciferol is that it can produce "hypercalcemia,which results in systemic calcification of soft tissue, leading tokidney failure,cardiacabnormalities,hypertension,CNS depression, and GI upset. Signs generally develop within18–36 hof ingestion and can include depression,loss of appetite,polyuria,andpolydipsia."[17]High-dose cholecalciferol will tend to rapidly accumulate inadiposetissue yet release more slowly[49]which will tend to delay time of death for several days from the time that high-dose bait is introduced.[48]

In New Zealand,possumshave become a significant pest animal. For possum control, cholecalciferol has been used as the active ingredient in lethal baits.[50]TheLD50is 16.8 mg/kg, but only 9.8 mg/kg if calcium carbonate is added to the bait.[51][52]Kidneys and heart are target organs.[53]LD50of 4.4 mg/kg has been reported in rabbits, with lethality to almost all rabbits ingesting doses greater than 15 mg/kg.[54]Toxicity has been reported across a wide range of cholecalciferol dosages, with LD50as high as 88 mg/kg or LDLoas low as 2 mg/kg reported for dogs.[55]

Researchers have reported that the compound is less toxic to non-target species than earlier generations of anticoagulant rodenticides (Warfarinandcongeners) orBromethalin,[56]and thatrelay toxicosis(poisoning by eating a poisoned animal) has not been documented.[17]Nevertheless, the same source reports that use of cholecalciferol inrodenticidesmay still pose a significant hazard to other animals, such as dogs and cats, when rodenticide bait or other forms of cholecalciferol are directly ingested.[17]

See also[edit]

References[edit]

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  55. ^Michael E.Peterson & Kerstin Fluegeman,Cholecalciferol (Topic Review),Topics in Companion Animal Medicine, Volume 28, Issue 1, February 2013, Pages 24-27.
  56. ^Kocher DK, Kaur G, Banga HS, Brar RS (2010). "Histopathological Changes in Vital Organs of House Rats Given Lethal Dose of Cholecalciferol (Vitamin D3)".Indian Journal of Animal Research.2(3): 193–6.ISSN0367-6722.Use of cholecalciferol as a rodenticide in bait lowered the risk of secondary poisoning and minimized the toxicity of non-target species

External links[edit]

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