β-Carotene is a strongly colored 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. 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 distinguished 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, pumpkins and sweet potatoes that colors them orange and is the most common form of carotene in plants. When used as a food coloring, it has the E number E160a.p119 The structure was deduced by Karrer et al. in 1930. In nature, β-carotene is a precursor (inactive form) to vitamin A via the action of beta-carotene 15,15'-monooxygenase. Isolation of β-carotene from fruits abundant in carotenoids is commonly done using column chromatography. It can also be extracted from the beta-carotene rich algae, Dunaliella Salina. 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. Being highly conjugated, it is deeply colored, and as a hydrocarbon lacking functional groups, it is very lipophilic.

Medical uses

β-Carotene has been used to treat various disorders such as erythropoietic protoporphyria. It has also been used to reduce the risk of breast cancer in women before menopause, and the risk of age-related macular degeneration (AMD).


Supplementation with β-carotene does not appear to decrease the risk cancer overall, nor specific cancers including: pancreatic, colorectal, prostate, breast, melanoma, or skin cancer generally. Evidence does not support a role for β-carotene in treating cancer. High levels of β-carotene may increase the risk of lung cancer in current and former smokers. This is likely because Beta-Carotene is unstable in cigarette smoke exposed lungs where it forms oxidized beta-carotene metabolites that can induce carcinogen-bioactiviating enzymes. Results are not clear for thyroid cancer. There is evidence that there remains a distinction between synthetic and natural beta-carotene in cancer treatment. Natural beta-carotene was shown to reverse premalignant gastric lesions while synthetic beta-carotene had no effect Beta-carotene has also been shown to protect from photoaging-associated mitrochondrial DNA mutations which may play a role in carcinogenesis


The effect of antioxidant vitamin supplementation on preventing and slowing the progression of age-related cataract has been studied. A Cochrane Review tested supplementation of β-carotene, Vitamin C, and Vitamin E, independently and combined on patients to examine differences in risk of cataract, cataract extraction, progression of cataract, and slowing the loss of visual acuity. However, these studies found no evidence of any protective effects afforded by β-carotene supplementation on preventing and slowing age-related cataract.

Side effects

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. Chronic, high doses of synthetic β-carotene supplements have been associated with a higher rate of lung cancer in smokers. 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. 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 colors such as annatto.


β-Carotene, 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), β-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 β-carotene decreases. Therefore, β-carotene is a very safe source of vitamin A and high intakes will not lead to hypervitaminosis A. Excess β-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 β-carotene leads to yellowish skin, but this is quickly reversible upon cessation of intake.

Drug interactions

β-Carotene can interact with medication used for lowering cholesterol. Taking them together can lower the effectiveness of these medications and is considered only a moderate interaction. β-Carotene should not be taken with Orlistat, a weight loss medication, as Orlistat can reduce the consumption of β-carotene by as much as 30%. Bile acid sequestrants and proton-pump inhibitors can also decrease absorption of β-carotene. Consuming alcohol with β-carotene can decrease its ability to convert to retinol and could possibly result in hepatotoxicity.

β-Carotene and lung cancer in smokers

Chronic high doses of β-carotene supplementation increases the probability of lung cancer in cigarette smokers. 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. 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-β (retinoic acid receptor beta), the complex binds AP1 (activator protein 1). AP1 is a transcription factor that binds to DNA and in downstream events promotes cell proliferation. Therefore, in the presence of retinoic acid, the retinoic acid:RAR-β complex binds to AP1 and inhibits 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.

Provitamin A activity

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 (α-tocopherol). One molecule of β-carotene can be cleaved by the intestinal enzyme β,β-carotene 15,15'-monooxygenase into two molecules of vitamin A.

Absorption efficiency is estimated to be between 9â€"22%. The absorption and conversion of carotenoids may depend on the form that the β-carotene is in (e.g., cooked vs. raw vegetables, or in a supplement), the intake of fats and oils at the same time, and the current stores of vitamin A and β-carotene in the body. Researchers list the following factors that determine the provitamin A activity of carotenoids:

  • Species of carotene
  • Molecular linkage
  • Amount in the meal
  • Matrix properties
  • Effectors
  • Nutrient status
  • Genetics
  • Host specificity
  • Interactions between factors

Symmetric and asymmetric cleavage

In the molecule chain between the two cyclohexyl rings β-carotene cleaves either symmetrically or asymmetrically. Symmetric cleavage with the enzyme β,β-carotene-15,15'-dioxygenase requires the antioxidant α-tocopherol. This symmetric cleavage gives two equivalent retinal molecules and each retinal molecule further reacts to give retinol (vitamin A) and retinoic acid. β-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.

Conversion factors

Since 2001, the US Institute of Medicine uses retinol activity equivalents (RAE) for their Dietary Reference Intakes, defined as follows:

Retinol activity equivalents (RAEs)

1 µg RAE = 1 µg retinol

1 µg RAE = 2 µg all-trans-β-carotene from supplements

1 µg RAE = 12 µg of all-trans-β-carotene from food

1 µg RAE = 24 µg α-carotene or β-cryptoxanthin from food

Retinol activity equivalent (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). RE was developed 1967 by the United Nations/World Health Organization Food and Agriculture Organization (FAO/WHO).

Another older unit of vitamin A activity is the international unit (IU). Like retinol equivalent, the international unit doesn't take into account carotenoids' variable absorption and conversion to vitamin A by humans as well as the more modern retinol activity equivalent. Unfortunately, food and supplement labels still generally use IU, but IU can be converted to the more useful retinol activity equivalent as follows:

International Units

1 µg RAE = 3.33 IU retinol 1 IU retinol = 0.3 μg RAE 1 IU β-carotene from supplements = 0.15 μg RAE 1 IU β-carotene from food = 0.05 μg RAE 1 IU α-carotene or β-cryptoxanthin from food = 0.025 μg RAE1

Dietary sources

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, pumpkin and papayas, and orange root vegetables such as carrots and yams. The color of β-carotene is masked by chlorophyll in green leafy vegetables such as spinach, kale, sweet potato leaves, and sweet gourd leaves. Vietnamese gac and crude palm oil have the highest content of β-carotene of any known plant source, 10 times higher than carrots, for example. However, gac is quite rare and unknown outside its native region of Southeast Asia, and crude palm oil is typically processed to remove the carotenoids before sale to improve the color and clarity.

The average daily intake of β-carotene is in the range 2â€"7 mg, as estimated from a pooled analysis of 500,000 women living in the USA, Canada, and some European countries.

The U.S. Department of Agriculture lists the following 10 foods to have the highest β-carotene content per serving.

Compendial status

  • British Pharmacopoeia


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