Beta-carotene is broken down in the mucosa of the small intestine and liver by beta-carotene dioxygenase to retinal which is a form of vitamin A. The function of this enzyme is vital as it decides if the beta-carotene is transformed to vitamin A or if it circulates in the plasma as beta-carotene. Less than a quarter of the ingested beta-carotene from root vegetables and about half of the beta-carotene from leafy green vegetables are converted to vitamin A.
A portion of the beta-carotene is converted to retinol in the wall of the small intestine, principally by its initial cleavage at the 15,15' double bond to form two molecules of retinal. Some of the retinal is further oxidized to retinoic acid; only one-half is reduced to retinol, which is then esterified and transported in the lymph. ...
Approximately 20 to 60% of beta-carotene is metabolized to retinaldehyde and then converted to retinol, primarily in the intestinal wall. A small amount of beta-carotene is converted to vitamin A in the liver. The proportion of beta-carotene converted to vitamin A diminishes inversely to the intake of beta-carotene, as long as the dosages are higher than one to two times the daily requirements. High doses of beta-carotene do not lead to abnormally high serum concentrations of vitamin A.
Beta carotene may be converted to 2 molecules of retinal by cleavage at the 15-15' double bond in the center of the molecule. Most of the retinal is reduced to retinol which is then conjugated with glucuronic acid and excreted in urine and feces. Some retinal may be further oxidized to retinoic acid which can be decarboxylated and further metabolized, secreted into bile, and excreted in feces as the glucuronide.
Two pathways have been suggested for the conversion of carotenoids to vitamin A in mammals, central cleavage and excentric cleavage. An enzyme, beta-carotenoid-15,15'-dioxygenase, has been partly purified from the intestines of several species and has been identified in several other organs and species. The enzyme, which converts beta-carotene into two molecules of retinal in good yield, requires molecular oxygen and is inhibited by sulfhydryl binding reagents and iron binding reagents. Most provitamin A carotenoids, including the beta-apo-carotenals, are cleaved to retinal by this enzyme. Its maximal activity in the rabbit is approximately 200 times that required to meet nutritional needs but is less than 50% of that expected to produce signs of vitamin A toxicity. Excentric cleavage unquestionably occurs in plants and some microorganisms and might occur in mammals. Thus far, however, carotenoid dioxygenase with excentric bond specificity has been identified in mammals, the yield of beta-apo-carotenals from beta-carotene in vivo and in vitro is very low, and beta-apo-carotenals are formed nonbiologically from beta-carotene.
◉ Summary of Use during Lactation:Beta-carotene is a plant pigment that is converted into vitamin A in the body. Maternal vitamin A requirements are increased during lactation, but there are no specific guidelines for increased beta-carotene intake or indications for high-dose supplementation in nursing mothers. Typical beta-carotene intake in a Western diet is 6 to 8 mg daily. Beta-carotene is a normal component of human colostrum and mature milk, where it contributes to antioxidant defenses in the neonate. A systematic review found that in infants younger than 6 months, those fed primarily human milk have greater blood carotenoid concentrations than those fed formula. Some evidence suggests that there is a correlation between beta-carotene and infant motor development in exclusively breastfed infants, but not in overall psychomotor performance. Beta-carotene supplementation during pregnancy and for 6 months postpartum in nursing mothers with poor diets in a resource-poor setting reduced the number of days of illness in the mothers, but does not reduce infant morbidity or mortality according to another study. The bioavailability of beta-carotene is dependent on the fat content of the meal and the form in which it is administered, with synthetic pharmaceutical forms having the best bioavailability. High-dose beta-carotene supplements lead to a slow increase in breastmilk beta-carotene concentrations, with an accumulation half-life of about 9 days. Levels drop towards baseline slowly over several weeks after discontinuation. In general, beta-carotene is well tolerated, although excessive maternal intake of beta-carotene can lead to a harmless, reversible discoloration of the breastfed infant's skin. In HIV-infected women, high-dose beta-carotene plus vitamin A supplementation increases the rate of HIV viral shedding into breastmilk and increases HIV infection in breastfed infants, although the mortality rate over the first 2 years of life is not increased. The viral shedding may be a result of an increase in subclinical mastitis caused by beta-carotene. Beta-carotene concentration in breastmilk is not affected by refrigeration, freezing, or low-temperature microwaving. The concentration does decrease when milk passes through a tube feeding system, regardless of light exposure.
Dietary supplements do not require extensive pre-marketing approval from the U.S. Food and Drug Administration. Manufacturers are responsible to ensure the safety, but do not need to prove the safety and effectiveness of dietary supplements before they are marketed. Dietary supplements may contain multiple ingredients, and differences are often found between labeled and actual ingredients or their amounts. A manufacturer may contract with an independent organization to verify the quality of a product or its ingredients, but that does not certify the safety or effectiveness of a product. Because of the above issues, clinical testing results on one product may not be applicable to other products. More detailed information about dietary supplements is available elsewhere on the LactMed Web site.
◉ Effects in Breastfed Infants:A nursing mother was eating 2 to 3 pounds of carrots a week as raw and cooked carrots. The mother's skin was yellow in color, but her sclera were clear. At 2 months of age, her breastfed infant was diagnosed as having jaundice because of a yellow coloration of the skin. Breastfeeding was discontinued and the infant's skin returned to a normal color. The mother continued her diet and examination of the maternal serum found elevated levels of beta-carotene which was probably the cause of her infant's skin discoloration.
HIV-infected women in Tanzania received 1 of 4 supplements during pregnancy and lactation in a series of studies. Groups received either multivitamins (thiamine, riboflavin, vitamin B6, niacin, vitamin B12, vitamin C, vitamin E, and folic acid), multivitamins plus vitamin A and beta-carotene, vitamin A and beta-carotene alone, or placebo daily. The beta-carotene dose was 30 mg. At 24 months of age, the multivitamin-supplemented group's infants had significantly better growth parameters than the other groups. One study found that the infants of mothers supplemented with vitamin A and beta-carotene had a higher rate of HIV transmission than those supplemented with multivitamins alone or placebo. After 6 months postpartum, women who received vitamin A plus beta-carotene had greater shedding of the HIV virus into breastmilk than women who had not; multivitamins without vitamin A and beta-carotene did not increase viral shedding. Beta-carotene appeared to have a shedding effect that was independent of vitamin A. One possible explanation comes from another similar study in which those who received vitamin A plus beta-carotene alone had a 45% increased risk of severe subclinical mastitis and those who received multivitamins plus vitamin A and beta-carotene had a 29% increased risk of severe subclinical mastitis.
Breastmilk samples were collected at the first, third and sixth months postpartum from 39 mother-infant pairs of exclusively breastfed infants. Psychomotor testing found a correlation between beta-carotene intake in breastmilk during the first 3 months of life and infant motor development, but not overall psychomotor development, at 6 months of life. Some long-chain polyunsaturated fatty acids, DHA, alpha-linolenic acid and total n-3 PUFAs, also correlated with motor development.
◉ Effects on Lactation and Breastmilk:Relevant published information was not found as of the revision date.
Cigarette smoking is associated with decreased plasma levels of ascorbate and beta-carotene, which indicates that the smoking related chronic inflammatory response leads to an imbalance of oxidant/antioxidant homeostasis and possible predisposition to oxidant inflicted tissue damage and disease.
Weanling male Sprague-Dawley rats were pair-fed beta-carotene (56.5 mg/L of diet) for 8 weeks, with and without ethanol. As expected, ethanol increased CYP2E1 (measured by Western blots) from 67 + or - 8 to 317 + or - 27 densitometric units (p < 0.001). Furthermore, beta-carotene potentiated the ethanol induction to 442 + or - 38 densitometric units (p < 0.01) with a significant interaction (p = 0.012). The rise was confirmed by a corresponding increase in the hydroxylation of p-nitrophenol, a specific substrate for CYP2E1, and by the inhibition with diethyl dithiocarbamate (50 microM). Beta-carotene alone also significantly induced CYP4A1 protein (328 + or - 49 vs. 158 + or - 17 densitometric units, p < 0.05). The corresponding CYP4A1 mRNA (measured by Northern blots) was also increased (p < 0.05) and there was a significant interaction of the two treatments (p = 0.015). The combination of ethanol and beta-carotene had no significant effect on either total cytochrome P-450 or CYP1A1/2, CYP2B, CYP3A, and CYP4A2/3 contents. Beta-carotene potentiates the CYP2E1 induction by ethanol in rat liver and also increases CYP4A1, which may, at least in part, explain the associated hepatotoxicity.
SULFITE-MEDIATED BETA-CAROTENE DESTRUCTION WAS INVESTIGATED; IT WAS INHIBITED BY ALPHA-TOCOPHEROL, 1,2-DIHYDROXYBENZENE-3,5-DISULFONIC ACID & BUTYLATED HYDROXYTOLUENE
After administration of beta-carotene, some of the administered dose is absorbed into the circulatory system unchanged and stored in the fat tissue. The coadministration of beta-carotene and a high-fat content diet is correlated to a better absorption of beta-carotene. The absorption is also dependent on the isomeric form of the molecule where the cis conformation seems to present a higher bioavailability. The absorption of beta-carotene is thought to be performed in 6-7 hours. The reported AUC of beta-carotene when administered orally from 0 to 440 hours after initial administration was reported to be 26.3 mcg.h/L. The maximal concentration of beta-carotene is attained in a dual pharmacokinetic profile after 6 hours and again after 32 hours with a concentration of 0.58 micromol/L.
The unabsorbed carotene is excreted in feces. It is also excreted in feces and urine as metabolites. The consumption of dietary fiber can increase the fecal excretion of fats and other fat-soluble compounds such as beta-carotene.
Carotenoids are absorbed and transported via lymphatics to the liver. They circulate in association with lipoproteins, and are found in liver, adrenal, testes, and adipose tissue, and can be converted to vitamin A in numerous tissues, including the liver. Some beta carotene is absorbed as such and circulates in association with lipoproteins; it apparently partitions into body lipids and can be converted to vitamin A in numerous tissues, including the liver.
3,4;3′,4′-Bisdehydro-β-carotene and 3,4-monodehydro-β-carotene are synthesized by building up the C40skeleton following the scheme C19 + C2 + C19 = C40. The synthesis of the symmetrical 3,4;3′,4′-bisdehydro-β-carotene is based on the use of two units of dehydro-β-C19-aldehyde. The asymmetrical 3,4-monodehydro-β-carotene is formed from one unit each of dehydro-β-C19-aldehyde and β-C19-aldehyde. 3,4;3′
通过按照方案C 19 + C 2 + C 19＝ C 40构筑C 40骨架，合成了3,4; 3'，4'-双氢-β-胡萝卜素和3,4-单氢-β-胡萝卜素。的对称3,4-合成; 3'，4'-bisdehydro-β胡萝卜素是基于使用的脱氢-β-C的两个单元19 -醛。非对称3,4- monodehydro-β胡萝卜素从一个单元中的每个的脱氢-β-C形成19 -醛和β-C 19 -醛。3,4; 3'，4'-双去氢-β-胡萝卜素比3,4-单去氢-β-胡萝卜素形成更亮的红色溶液。在生长试验中，前者显示出38％的β-胡萝卜素活性，而后者显示了75％的β-胡萝卜素活性。
A conjunctive diiodoheptaene for the synthesis of C2-symmetric carotenoids
作者：Noelia Fontán、Belén Vaz、Rosana Álvarez、Ángel R. de Lera
DOI：10.1039/c3cc38676g
日期：——
(2E,4E,6E,8E,10E,12E,14E)-2,15-Diiodo-6,11-dimethylhexadeca-2,4,6,8,10,12,14-heptaene, prepared by homometathesis, has been used in palladium-catalyzed Suzuki and Stille cross-coupling reactions with the appropriate partners to construct the C2-symmetric carotenoids β,β-carotene, lycopene, synechoxanthin and 4,4′-diapo-ψ,ψ-carotene-4,4′-dial.
Dialdehyde compound, preparation method thereof, and synthetic method of carotenoids using the same
申请人：Koo Sang Ho
公开号：US20090318732A1
公开（公告）日：2009-12-24
The novel C dialdehyde compound which can be efficiently utilized in the synthesis of carotenoid compounds based on the sulfone chemistry, the preparation method of the same, and the expeditious and practical synthetic processes for lycopene and β-carotene by the use of the above novel compound are disclosed. The syntheses of lycopene and β-carotene are characterized by the processes of the coupling reaction between two equivalents of geranyl sulfone or cyclic geranyl sulfone and the above C dialdehyde, the functional group transformation reactions of the diol in the resulting C 40 coupling products to X's (either halogens or ethers), and the double elimination reactions of the functional groups of the benzenesulfonyl and X to produce the fully conjugated polyene chain of the carotenoids.
[EN] ClO DIALDEHYDE, SYNTHETIC METHOD THEREOF, AND SYNTHETIC METHOD OF BETA-CAROTENE USING THE SAME<br/>[FR] DIALDEHYDE C10, PROCEDE DE SYNTHESE ASSOCIE, ET PROCEDE DE SYNTHESE DE BETA-CAROTENE ASSOCIE
申请人：KOO SANGHO
公开号：WO2006038764A1
公开（公告）日：2006-04-13
The novel intermediate compound which can be efficiently utilized in the synthesis of carotenoid compounds based on the sulfone chemistry, the preparation method of the same, and the practical synthetic process for preparing β-carotene by the use of the above novel compound are disclosed. The synthesis of β-carotene is characterized by the double elimination reactions of the C40 compound containing both the benzenesulfonyl group and the group X (either halogen or ether), which can be prepared by the coupling reaction of the novel C10 dialdehyde with two equivalents of the C15 allylic sulfone, followed by the functional group transformation of the resulting C40 diol either to the corresponding halide or to the ether, to produce the fully conjugated polyene chain.
