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| Names | |
|---|---|
| IUPAC name β,β-Carotene | |
| Systematic IUPAC name 1,1′-[(1E,3E,5E,7E,9E,11E,13E,15E,17E)-3,7,12,16-Tetramethyloctadeca-1,3,5,7,9,11,13,15,17-nonaene-1,18-diyl]bis(2,6,6-trimethylcyclohex-1-ene) | |
| Other names | |
| Identifiers | |
3D model (JSmol) | |
| 1917416 | |
| ChEBI | |
| ChEMBL | |
| ChemSpider |
|
| ECHA InfoCard | 100.027.851 |
| EC Number |
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| E number | E160a(colours) |
| KEGG | |
| UNII | |
| |
| |
| Properties | |
| C40H56 | |
| Molar mass | 536.888 g·mol−1 |
| Appearance | Dark orange crystals |
| Density | 1.00 g/cm3[4] |
| Melting point | 183 °C (361 °F; 456 K)[4] decomposes[6] |
| Boiling point | 654.7 °C (1,210.5 °F; 927.9 K) at 760 mmHg (101324 Pa) |
| Insoluble | |
| Solubility | Soluble inCS2,benzene,CHCl3,ethanol Insoluble inglycerin |
| Solubility indichloromethane | 4.51 g/kg (20 °C)[5] = 5.98 g/L (given BCM density of 1.3266 g/cm3 at 20°C) |
| Solubility inhexane | 0.1 g/L |
| logP | 14.764 |
| Vapor pressure | 2.71·10−16 mmHg |
Refractive index (nD) | 1.565 |
| Pharmacology | |
| A11CA02 (WHO) D02BB01 (WHO) | |
| Hazards | |
| GHS labelling: | |
 | |
| Warning | |
| H315,H319,H412 | |
| P264,P273,P280,P302+P352,P305+P351+P338,P321,P332+P313,P337+P313,P362,P501 | |
| NFPA 704 (fire diamond) | |
| Flash point | 103 °C (217 °F; 376 K)[6] |
Except where otherwise noted, data are given for materials in theirstandard state (at 25 °C [77 °F], 100 kPa). | |
β-Carotene (beta-carotene) is anorganic, strongly colored red-orangepigment abundant in fungi,[7] plants, and fruits. It is a member of thecarotenes, which areterpenoids (isoprenoids), synthesized biochemically from eightisoprene units and thus having 40carbons.
Dietary β-carotene is a provitamin A compound, converting in the body toretinol (vitamin A).[8] In foods, it has rich content incarrots,pumpkin,spinach, andsweet potato.[8] It is used as adietary supplement and may be prescribed to treaterythropoietic protoporphyria, an inherited condition of sunlight sensitivity.[9]
β-carotene is the most common carotenoid in plants.[8] When used as afood coloring, it has theE number E160a.[10]: 119 The structure was deduced in 1930.[11]
Isolation of β-carotene from fruits abundant in carotenoids is commonly done using columnchromatography. It is industrially extracted from richer sources such as the algaeDunaliella salina.[12] The separation of β-carotene from the mixture of other carotenoids is based on the polarity of a compound. β-Carotene is a non-polar compound, so it is separated with a non-polar solvent such ashexane.[13] Being highlyconjugated, it is deeply colored, and as ahydrocarbon lacking functional groups, it islipophilic.
Plant carotenoids are the primary dietary source ofprovitamin A worldwide, with β-carotene as the best-known provitamin A carotenoid.[8] Others includeα-carotene andβ-cryptoxanthin.[8] Carotenoid absorption is restricted to theduodenum of thesmall intestine. One molecule of β-carotene can be cleaved by the intestinal enzymeβ,β-carotene 15,15'-monooxygenase into two molecules of vitamin A.[8][14][15]
As part of the digestive process, food-sourced carotenoids must be separated from plant cells and incorporated into lipid-containing micelles to be bioaccessible to intestinalenterocytes.[8] If already extracted (or synthetic) and then presented in an oil-filled dietary supplement capsule, there is greater bioavailability compared to that from foods.[16]
At the enterocyte cell wall, β-carotene is taken up by the membrane transporter protein scavenger receptor class B, type 1 (SCARB1). Absorbed β-carotene is then either incorporated as such intochylomicrons or first converted to retinal and then retinol, bound toretinol binding protein 2, before being incorporated into chylomicrons.[8] The conversion process consists of one molecule of β-carotene cleaved by the enzymebeta-carotene 15,15'-dioxygenase, which is encoded by the BCO1 gene, into two molecules of retinal.[8] When plasma retinol is in the normal range the gene expression for SCARB1 and BCO1 are suppressed, creating a feedback loop that suppresses β-carotene absorption and conversion.[16]
The majority of chylomicrons are taken up by the liver, then secreted into the blood repackaged intolow density lipoproteins (LDLs).[8] From these circulating lipoproteins and the chylomicrons that bypassed the liver, β-carotene is taken into cells via receptor SCARB1. Human tissues differ in expression of SCARB1, and hence β-carotene content. Examples expressed as ng/g, wet weight: liver=479, lung=226, prostate=163 and skin=26.[16]
Once taken up by peripheral tissue cells, the major usage of absorbed β-carotene is as a precursor to retinal via symmetric cleavage by the enzyme beta-carotene 15,15'-dioxygenase, which is encoded by the BCO1 gene.[8] A lesser amount is metabolized by the mitochondrial enzyme beta-carotene 9',10'-dioxygenase, which is encoded by the BCO2 gene. The products of this asymmetric cleavage are twobeta-ionone molecules and rosafluene. BCO2 appears to be involved in preventing excessive accumulation of carotenoids; a BCO2 defect in chickens results in yellow skin color due to accumulation in subcutaneous fat.[17][18]
For counting dietary vitamin A intake, β-carotene may be converted either using the newer retinol activity equivalents (RAE) or the older international unit (IU).[8]
Since 2001, the US Institute of Medicine uses retinol activity equivalents (RAE) for their Dietary Reference Intakes, defined as follows:[8][19]
RAE takes into account carotenoids' variable absorption and conversion to vitamin A by humans better than and replaces the older retinol equivalent (RE) (1 μg RE = 1 μg retinol, 6 μg β-carotene, or 12 μg α-carotene or β-cryptoxanthin).[19] RE was developed 1967 by the United Nations/World Health Organization Food and Agriculture Organization (FAO/WHO).[20]
Another older unit of vitamin A activity is the international unit (IU).[8] Like retinol equivalent, the international unit does not take into account carotenoid variable absorption and conversion to vitamin A by humans, as well as the more modern retinol activity equivalent. Food and supplement labels still generally use IU, but IU can be converted to the more useful retinol activity equivalent as follows:[19]
The average daily intake of β-carotene is in the range 2–7 mg, as estimated from a pooled analysis of 500,000 women living in the US, Canada, and some European countries.[21] Beta-carotene is found in many foods and is sold as adietary supplement.[8] β-Carotene contributes to the orange color of many different fruits and vegetables.Vietnamesegac (Momordica cochinchinensis Spreng.) and crudepalm oil are particularly rich sources, as are yellow and orange fruits, such ascantaloupe,mangoes,pumpkin, andpapayas, and orangeroot vegetables such ascarrots andsweet potatoes.[8]
The color of β-carotene is masked bychlorophyll in greenleaf vegetables such asspinach,kale, sweet potato leaves, and sweetgourd leaves.[8][22]
The U.S. Department of Agriculture lists foods high in β-carotene content:[23]
| Food | Beta-carotene Milligramsper 100 g |
|---|---|
| Sweet potato, skinned, boiled | 9.4 |
| Carrot juice | 9.3 |
| Carrots, raw or boiled | 9.2 |
| Kale, boiled | 8.8 |
| Pumpkin, canned | 6.9 |
| Spinach, canned | 5.9 |
Government and non-government organizations have not set a dietary requirement for β-carotene.[16]
Excess β-carotene is predominantly stored in the fat tissues of the body.[8] The most common side effect of excessive β-carotene consumption iscarotenodermia, a physically harmless condition that presents as a conspicuousorangeskin tint arising from deposition of the carotenoid in the outermost layer of theepidermis.[8][9][16][24]
Carotenoderma, also referred to as carotenemia, is a benign and reversible medical condition where an excess of dietary carotenoids results in orange discoloration of the outermost skin layer.[8] It is associated with a high blood β-carotene value. This can occur after a month or two of consumption of beta-carotene rich foods, such as carrots, carrot juice, tangerine juice, mangos, or in Africa, red palm oil. β-carotene dietary supplements can have the same effect. The discoloration extends to palms and soles of feet, but not to thewhite of the eye, which helps distinguish the condition fromjaundice. Carotenodermia is reversible upon cessation of excessive intake.[25] Consumption of greater than 30 mg/day for a prolonged period has been confirmed as leading to carotenemia.[16][26]
At theenterocyte cell wall, β-carotene is taken up by the membrane transporter protein scavenger receptor class B, type 1 (SCARB1). Absorbed β-carotene is then either incorporated as such into chylomicrons or first converted to retinal and then retinol, bound toretinol binding protein 2, before being incorporated into chylomicrons. The conversion process consists of one molecule of β-carotene cleaved by the enzymebeta-carotene 15,15'-dioxygenase, which is encoded by the BCO1 gene, into two molecules of retinal. When plasma retinol is in the normal range the gene expression for SCARB1 and BCO1 are suppressed, creating a feedback loop that suppresses absorption and conversion. Because of these two mechanisms, high intake will not lead tohypervitaminosis A.[16]
β-Carotene can interact with medication used for loweringcholesterol.[8] Taking them together can lower the effectiveness of these medications and is considered only a moderate interaction.[8]Bile acid sequestrants andproton-pump inhibitors can decrease absorption of β-carotene.[27] Consuming alcohol with β-carotene can decrease its ability to convert to retinol and could possibly result inhepatotoxicity.[28] Research on animal feeds, suggests that β-Carotene might act as an "antivitamin D" that counteracts the availability inforages ofvitamin D.[29][30]
Chronic high doses of β-carotene supplementation increases the probability of lung cancer insmokers[8][31] while its natural vitamer, retinol, increases lung cancer in smokers and nonsmokers. The effect is specific to supplementation dose as nolung damage has been detected in those who are exposed to cigarette smoke and who ingest a physiological dose of β-carotene (6 mg), in contrast to high pharmacological dose (30 mg).[8][32]
Increases in lung cancer have been attributed to the tendency of β-carotene to oxidize,[33] yet based on the pharmacokinetics of β-carotene absorption and transport through the intestine and the lack of specific β-carotene transporters, it is unlikely that β-carotene reaches the lung of smokers in sufficient quantities.[34] Additional research is required to understand the link between the increased risk of cancer and all-cause mortality following β-carotene supplementation.
Additionally, supplemental, high-dose β-carotene may increase the risk ofprostate cancer,intracerebral hemorrhage, and cardiovascular and total mortality irrespective of smoking status.[8][9]
β-carotene is industrially made either by total synthesis (seeRetinol § Industrial synthesis) or by extraction from biological sources such as vegetables, microalgae (especiallyDunaliella salina), and genetically-engineered microbes. The synthetic path is low-cost and high-yield.[35]
Medical authorities generally recommend obtaining beta-carotene from food rather than dietary supplements.[8] A 2013 meta-analysis ofrandomized controlled trials concluded that high-dosage (≥9.6 mg/day) beta-carotene supplementation is associated with a 6% increase in the risk of all-causemortality, while low-dosage (<9.6 mg/day) supplementation does not have a significant effect on mortality.[36] Research is insufficient to determine whether a minimum level of beta-carotene consumption is necessary for human health and to identify what problems might arise from insufficient beta-carotene intake.[37] However, a 2018 meta-analysis mostly ofprospective cohort studies found that both dietary andcirculating beta-carotene are associated with a lower risk of all-cause mortality. The highest circulating beta-carotene category, compared to the lowest, correlated with a 37% reduction in the risk of all-cause mortality, while the highest dietary beta-carotene intake category, compared to the lowest, was linked to an 18% decrease in the risk of all-cause mortality.[38]
Age-related macular degeneration (AMD) represents the leading cause of irreversible blindness in elderly people. AMD is an oxidative stress, retinal disease that affects the macula, causing progressive loss of central vision.[39] β-carotene content is confirmed in human retinal pigment epithelium.[16] Reviews reported mixed results for observational studies, with some reporting that diets higher in β-carotene correlated with a decreased risk of AMD whereas other studies reporting no benefits.[40] Reviews reported that for intervention trials using only β-carotene, there was no change to risk of developing AMD.[8][40][41]
A meta-analysis concluded that supplementation with β-carotene does not appear to decrease the risk of cancer overall, nor specific cancers including: pancreatic, colorectal, prostate, breast, melanoma, or skin cancer generally.[8][42] High levels of β-carotene may increase the risk of lung cancer in current and former smokers.[8][43] Results are not clear for thyroid cancer.[44]
ACochrane review looked at supplementation of β-carotene, vitamin C, and vitamin E, independently and combined, on people to examine differences in risk ofcataract, cataract extraction, progression of cataract, and slowing the loss of visual acuity. These studies found no evidence of any protective effects afforded by β-carotene supplementation on preventing and slowing age-related cataract.[45] A second meta-analysis compiled data from studies that measured diet-derived serum beta-carotene and reported a not statistically significant 10% decrease in cataract risk.[46]
High doses of β-carotene (up to 180 mg per day) may be used as a treatment forerythropoietic protoporphyria, a rare inherited disorder of sunlight sensitivity, without toxic effects.[8][9]
Foods rich in carotenoid dyes show discoloration upon drying. This is due tothermal degradation of carotenoids, possibly viaisomerization and oxidation reactions.[47]
| Authority control databases: National |
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