| β-Carotene | |
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beta,beta-Carotene |
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Other names
Betacarotene β-Carotene[1] |
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| Identifiers | |
| CAS number | 7235-40-7 |
| PubChem | 573 |
| ChemSpider | 4444129 |
| UNII | 01YAE03M7J |
| ChEBI | CHEBI:17579 |
| ChEMBL | CHEMBL1293 |
| ATC code | A11 |
| Jmol-3D images | Image 1 |
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| Properties | |
| Molecular formula | C40H56 |
| Molar mass | 536.87 g mol−1 |
| Exact mass | 536.438201792 g mol-1 |
| Appearance | Dark orange crystals |
| Density | 0.94(6) g cm-3 |
| Melting point |
180-182 °C, 453-455 K, 356-360 °F |
| Boiling point |
633-677 °C, 906-950 K, 1171-1251 °F (at 760 Torr[1]) |
| log P | 14.764 |
| Hazards | |
| Flash point | 103 °C[2] |
| (verify) (what is: /?) Except where noted otherwise, data are given for materials in their standard state (at 25 °C, 100 kPa) |
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| Infobox references | |
β-Carotene is a strongly-coloured red-orange pigment abundant in plants and fruits. It is an organic compound and chemically is classified as a hydrocarbon and specifically as a terpenoid (isoprenoid), reflecting its derivation from isoprene units. β-Carotene is biosynthesized from geranylgeranyl pyrophosphate.[3] It is a member of the carotenes, which are tetraterpenes, synthesized biochemically from eight isoprene units and thus having 40 carbons. Among this general class of carotenes, β-Carotene is distinquished by having beta-rings at both ends of the molecule. Absorption of β-Carotene is enhanced if eaten with fats, as carotenes are fat soluble.
Carotene is the substance in carrots that colours them orange and is the most common form of carotene in plants. When used as a food colouring, it has the E number E160a.[4]p119
The structure was deduced by Karrer et al. in 1930.[5] In nature, β-carotene is a precursor (inactive form) to vitamin A via the action of beta-carotene 15,15'-monooxygenase.[3]
Isolation of β-carotene from fruits abundant in carotenoids is commonly done using column chromatography. 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 as hexane.[6] Being highly conjugated, it is deeply colored, and as a hydrocarbon lacking functional groups, it is very lipophilic.
Contents |
Plant carotenoids are the primary dietary source of provitamin A worldwide, with β-carotene as the most well-known provitamin A carotenoid. Others include α-carotene and β-cryptoxanthin. Carotenoid absorption is restricted to the duodenum of the small intestine and dependent on Class B scavenger receptor (SR-B1) membrane protein, which are also responsible for the absorption of vitamin E (alpha-tocopherol).[7] One molecule of β-carotene can be cleaved by the intestinal enzyme beta,beta-carotene 15,15'-monooxygenase into two molecules of vitamin A.[8]
Absorption efficiency is estimated to be between 9-22%. The absorption and conversion of carotenoids may depend on the form that the β-carotene is in (cooked vs. raw vegetables, in a supplement), intake of fats and oils at the same time, and current stores of vitamin A and β-carotene in the body. Researchers list the following factors that determine the provitamin A activity of carotenoids:[9]
In the molecule chain between the two cyclohexyl rings β-carotene cleaves either symmetrically or asymmetrically. Symmetric cleavage with the enzyme beta,beta-carotene-15,15'-dioxygenase requires the antioxidant alpha-tocopherol.[10] This symmetric cleavage gives two equivalent retinal molecules and each retinal molecule further reacts to give retinol (vitamin A) and retinoic acid. Beta-carotene is also asymmetrically cleaved into two asymmetric products. The product of asymmetric cleavage is β-apocarotenal (8',10',12'). Asymmetric cleavage reduces the level of retinoic acid significantly.[11]
Until recently, vitamin A activity in foods was expressed as international units (IU). This is still the measurement generally used on food and supplement labels. However, it is difficult to calculate the total vitamin A activity in the diet in terms of IU, because both the absorption and conversion of carotenoids, as compared with retinol, are variable. The unit retinol equivalent (RE) was developed by the Food and Agriculture Organization of the United Nations/World Health Organization (FAO/WHO) in 1967.[12] More recently in 2001, the US Institute of Medicine proposed retinol activity equivalents (RAE) for their Dietary Reference Intakes.[13]
1 RE = 3.33 IU vitamin A activity from retinol
1 RE = 10 IU vitamin A activity from β-carotene
(In Canada, Health Canada sets 1 RE = 6.667 IU from β-carotene.[14])
1 RE = 1 µg retinol
1 RE = 6 µg β-carotene (In Canada, Heath Canada sets 1 RE = 2 µg β-carotene.[14])
1 RE = 12 µg other provitamin A carotenoids
1 RAE = 1 µg retinol
1 RAE = 2 µg all-trans-β-carotene as a supplement
1 RAE = 12 µg of all-trans-β-carotene in a food matrix
1 RAE = 24 µg other provitamin A carotenes in a food matrix
β-Carotene contributes to the orange color of many different fruits and vegetables. Vietnamese gac (Momordica Cochinchinensis Spreng.) and crude palm oil are particularly rich sources, as are yellow and orange fruits, such as cantaloupe, mangoes and papayas, orange root vegetables such as carrots and yams and in green leafy vegetables such as spinach, kale, sweet potato leaves, and sweet gourd leaves. Vietnamese gac and crude palm oil have by far the highest content of β-carotene of any known fruit or vegetable, 10 times higher than carrots for example. However, gac is quite rare and unknown outside its native region of SE Asia, and crude palm oil is typically processed to remove the cartenoids before sale to improve the color and clarity.
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 USA, Canada and some European countries.[15]
The U.S. Department of Agriculture lists the following 10 foods to have the highest β-carotene content per serving.[16]
| Item | Grams per serving | Serving size | Milligrams β-carotene per serving | Milligrams β-carotene per 100 g |
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| Carrot juice, canned | 236 | 1 cup | 22.0 | 9.3 |
| Pumpkin, canned, without salt | 245 | 1 cup | 17.0 | 6.9 |
| Sweet potato, cooked, baked in skin, without salt | 146 | 1 potato | 16.8 | 11.5 |
| Sweet potato, cooked, boiled, without skin | 156 | 1 potato | 14.7 | 9.4 |
| Spinach, frozen, chopped or leaf, cooked, boiled, drained, without salt | 190 | 1 cup | 13.8 | 7.2 |
| Carrots, cooked, boiled, drained, without salt | 156 | 1 cup | 13.0 | 8.3 |
| Spinach, canned, drained solids | 214 | 1 cup | 12.6 | 5.9 |
| Sweet potato, canned, vacuum pack | 255 | 1 cup | 12.2 | 4.8 |
| Carrots, frozen, cooked, boiled, drained, without salt | 146 | 1 cup | 12.0 | 8.2 |
| Collards, frozen, chopped, cooked, boiled, drained, without salt | 170 | 1 cup | 11.6 | 6.8 |
The most common side effect of excessive β-carotene consumption is carotenodermia, a physically harmless condition that presents as a conspicuous orange skin tint arising from deposition of the carotenoid in the outermost layer of the epidermis.[17] Chronic, high doses of synthetic β-carotene supplements have been associated with increased rate of lung cancer among those who smoke.[18] Additionally, supplemental β-carotene may increase the risk of prostate cancer, intracerebral hemorrhage, and cardiovascular and total mortality in people who smoke cigarettes or have a history of high-level exposure to asbestos.[19]
β-Carotene is stored in the liver and many other organs ("golden ovaries"). Heavy consumption of synthetic β-carotene additive from a variety of foods, plus from natural sources, may result in saturating the liver's storage capacity for fat soluble vitamins, so that reserves of other fat soluble vitamins, e.g. vitamin D and vitamin A, are not created - in countries far from the Equator, the summer storage of vitamin D, to be drawn upon during the darker winter, may be particularly important, not least in preventing osteoporosis and other vitamin D-deficiency related problems. In many cases the food color annatto can be used instead of β-carotene, and is not deposited in the body.
β-Carotene has a high tendency to oxidize, more so than most food fats, and may thus to some extent hasten oxidation more than other food colours such as annatto.
Betacarotene, a precursor form of vitamin A typical of vegetable sources such as carrots, is selectively converted into retinoids, so it does not cause hypervitaminosis A; however, overconsumption can cause carotenosis, a benign condition in which the skin turns orange.
The proportion of carotenoids absorbed decreases as dietary intake increases. Within the intestinal wall (mucosa), beta-carotene is partially converted into vitamin A (retinol) by an enzyme, dioxygenase. This mechanism is regulated by the individual's vitamin A status. if the body has enough vitamin A, the conversion of beta-carotene decreases. Therefore, beta-carotene is a very safe source of vitamin A and high intakes will not lead to hypervitaminosis A. Excess beta-carotene is predominantly stored in the fat tissues of the body. The adult's fat stores are often yellow from accumulated carotene while the infant's fat stores are white. Excessive intake of beta-carotene leads to yellowish skin, but this is quickly reversible upon cessation of intake.[20]
Rat studies show that the body cannot convert such stored β-carotene into vitamin A, even if a deficit develops.
Chronic high doses of β-carotene supplementation increases the probability of lung cancer in cigarette smokers according to a study, although the validity of this statement has been put into question.[21] The effect is specific to supplementation dose as no lung damage has been detected in those who are exposed to cigarette smoke and who ingest a physiologic dose of β-carotene (6 mg), in contrast to high pharmacologic dose (30 mg). Therefore, the oncology from β-carotene is based on both cigarette smoke and high daily doses of β-carotene.[22]
There have been at least two suggestions for the mechanism for the observed harmful effect of high-dose β-carotene supplementation in this group. None has so-far gained wide acceptance.
A common explanation of the high dose effect is that when retinoic acid is liganded to RAR-beta (retinoic acid receptor beta), the complex binds AP1 (activator protein 1). AP1 is a transcription factor that binds to DNA and in downstream events promote cell proliferation. Therefore, in the presence of retinoic acid, the retinoic acid:RAR-beta complex binds to AP1 and inhibit AP-1 from binding to DNA. In that case, AP1 is no longer expressed, and cell proliferation does not occur. Cigarette smoke increases the asymmetric cleavage of β-carotene, decreasing the level of retinoic acid significantly. This can lead to a higher level of cell proliferation in smokers, and consequently, a higher probability of lung cancer.
Another β-carotene breakdown product suspected of causing cancer at high dose is trans-β-apo-8'-carotenal (common apocarotenal), which has been found in one study to be mutagenic and genotoxic in cell cultures which do not respond to β-carotene itself.[23]
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