Carotenoid Transport Research Articles

Nutritional factors and visual function in premature infants.

Approximately 5-7% of all infants are born prematurely, and birth before 37 weeks is the most common cause of neonatal mortality, morbidity and long-term disability. Premature infants are poorly equipped for life outside the womb, and oxidant stress has been implicated in the aetiology of visual impairment in these infants, who are often exposed to increased O2 concentrations and high light intensity in neonatal units. The carotenoids lutein and zeaxanthin, which give the macular area of the eye its yellow colour, are located in the retinal pigment epithelium of the eye, and are believed to play a role in protecting it against oxidative and light damage. The macular pigments are of dietary origin, and green leafy vegetables are the primary source of lutein and zeaxanthin. Lutein is one of the five most common carotenoids found in the diet. There is current interest in the macular pigment in relation to age-related macular degeneration, but these pigments may also have a protective role in the retinal pigment epithelium of the newborn infant. Little information is available on blood lutein and zeaxanthin levels in neonates. Levels of lutein in human milk are two to three times higher than those of beta-carotene, whereas their concentrations in the mothers' blood are approximately the same. Human milk is the main dietary source of lutein and zeaxanthin for infants until weaning occurs. The biochemical mechanisms which mediate the transport of the macular carotenoids into the eye are not known, but tubulin has been identified as the major carotenoid-binding protein, and may play a role in the physiology of the macula.

DCCD inhibits the reactions of the iron-sulfur protein in Rhodobacter sphaeroides chromatophores.

N,N'-dicyclohexylcarbodiimide (DCCD) has been reported to inhibit proton translocation by cytochrome bc(1) and b(6)f complexes without significantly altering the rate of electron transport, a process referred to as decoupling. To understand the possible role of DCCD in inhibiting the protonogenic reactions of cytochrome bc(1) complex, we investigated the effect of DCCD modification on flash-induced electron transport and electrochromic bandshift of carotenoids in Rb. sphaeroides chromatophores. DCCD has two distinct effects on phase III of the electrochromic bandshift of carotenoids reflecting the electrogenic reactions of the bc(1) complex. At low concentrations, DCCD increases the magnitude of the electrogenic process because of a decrease in the permeability of the membrane, probably through inhibition of F(o)F(1). At higher concentrations (>150 microM), DCCD slows the development of phase III of the electrochromic shift from about 3 ms in control preparations to about 23 ms at 1.2 mM DCCD, without significantly changing the amplitude. DCCD treatment of chromatophores also slows down the kinetics of flash-induced reduction of both cytochromes b and c, from 1.5-2 ms in control preparations to 8-10 ms at 0.8 mM DCCD. Parallel slowing of the reduction of both cytochromes indicates that DCCD treatment modifies the reaction of QH(2) oxidation at the Q(o) site. Despite the similarity in the kinetics of both cytochromes, the onset of cytochrome c re-reduction is delayed 1-2 ms in comparison to cytochrome b reduction, indicating that DCCD inhibits the delivery of electrons from quinol to heme c(1). We conclude that DCCD treatment of chromatophores leads to modification of the rate of Q(o)H(2) oxidation by the iron-sulfur protein (ISP) as well as the donation of electrons from ISP to c(1), and we discuss the results in the context of the movement of ISP between the Q(o) site and cytochrome c(1).

Canthaxanthin saturation of serum lipoproteins from immature rainbow trout ( Oncorhynchus mykiss)

Lipoproteins from immature rainbow trout serum fed a diet containing 100 mg cantaxanthin kg −1 of feed during 8 days were separated by ultracentrifugation. Canthaxanthin in the lipoprotein fraction amounted to 1.2, 1.8, 0.7 μg of canthaxanthin ml −1 of serum for VLDL, LDL, and HDL, respectively. Canthaxanthin, previously dissolved in ethyl ether, was added slowly (50 μl ml −1 of lipoprotein at a time) while gently stirring and evaporating the ethyl ether with N 2. After saturation, the canthaxanthin content in the lipoprotein increased about 100-fold, to 80.6, 152.8, 145.7 μg of canthaxanthin ml −1 serum for VLDL, LDL and HDL, respectively. It is concluded that the binding capacity of lipoproteins is not a limiting factor for carotenoid transport in trout.

Low pH enhances the transfer of carotene from carrot juice to olive oil.

A current model for carotenoid transport and absorption in the gut proposes an initial solubilization in the oil phase of dietary emulsions followed by incorporation of the carotenoids in mixed bile salt micelles. To assess the relevance of the first stage of this model to what is observed in vivo we have examined the transfer of carotene from carrot juice to olive oil. Increased acidity enhanced the transfer from both whole juice and carotene crystals isolated from carrot chromoplasts. The transfer was significantly slower from whole juice. By using exogenous beta-carotene and measuring its transfer to oil in the presence and absence of carrot juice we have demonstrated that the inhibition of the transfer in juice arises, at least in part, from soluble juice factors. The inhibition is relieved by a fall in pH, which leads to lowering of the electric potential at the oil/aqueous phase interface and aggregation of carrot tissue including crystalline carotene. Under conditions of low pH, oil droplets adhere to the tissue aggregates, allowing carotene to pass into the oil. Our results provide an explanation for why carotene absorption in vivo is depressed by conditions of low gastric acidity.

Absorption, metabolism, and transport of carotenoids

Carotenoids are currently under intense scrutiny regarding their potential to modulate chronic disease risk and prevent vitamin A deficiency, and renewed emphasis has been placed on achieving a better understanding of the metabolic fate of these compounds in humans. The development of new animal models, and use of human metabolic studies and stable tracer methods have greatly improved our knowledge of how carotenoids are absorbed, metabolized, and transported to tissues; however, many important issues remain unresolved. For example, intestinal uptake of carotenoids occurs by passive diffusion, but the lumenal or intracellular factors limiting this process are obscure. The intestinal mucosa plays a key role in the metabolism of provitamin A carotenoids such as beta-carotene, thus greatly influencing their bioavailability. Most recent evidence supports a central oxidation mechanism of cleavage of beta-carotene to retinal in the intestinal mucosa, but the extent and site(s) of postabsorptive metabolism in the human is unknown. While the human and other species clearly absorb non-provitamin A carotenoids, little is known of the extent and pathways of their metabolism and elimination. The metabolic fate of cis isomers of beta-carotene is a subject of recent interest, since 9-cis retinoic acid can apparently be formed from 9-cis beta-carotene in vitro and in vivo. Substantial cis-trans isomerization of at least small oral doses of 9-cis beta-carotene occurs in the human, although the site of isomerization is not yet known. Carotenoids are transported in plasma exclusively by lipoproteins, with the distribution among lipoprotein classes determined in large part by the physical properties of the carotenoid. The consequences of differential distribution in terms of tissue uptake and retention are not clear at present. Improved knowledge of the metabolic fate of carotenoids will assist in the development and testing of hypotheses regarding their potential to influence biological processes in the human.

Interspecific Variation in Plasma Hue in Relation to Carotenoid Plumage Pigmentation

Much of the bright yellow, orange, and red coloration of plumage results from carotenoid pigmentation (Brush 1978, Goodwin 1984). Carotenoids are unique among plumage pigments in that they cannot be synthesized by birds de novo; they must be ingested (Goodwin 1984, Brush 1978, 1990). An understanding of carotenoid pigmentation, therefore, requires an understanding of how birds get carotenoids from food into developing feathers. Unfortunately, the processes of carotenoid uptake, transport, and metabolism remain poorly understood (for reviews, see Brush 1978, 1990), with carotenoid transport perhaps the least studied aspect of carotenoid pigmentation (Brush 1990). To get from food in the gut to growing feathers, carotenoids must be transported in the blood. Trams (1969) was among the first to determine the carotenoid content of blood in relation to plumage coloration. He compared the blood of bright-red-plumaged Scarlet Ibises (Eudocimus ruber) with the blood of closely related but white-plumaged White Ibises (E. albus). As predicted, the blood of Scarlet Ibises contained much greater concentrations of red carotenoid pigments, as well as greater concentrations of a high-density lipoprotein that Trams (1969) speculated was the carrier protein for the carotenoids. Trams' study was conducted with birds that were not molting and, thus, at a time when carotenoid pigments in the blood would not be of use to the birds as feather

ChemInform Abstract: Absorption, Transport, and Metabolism of Carotenoids in Humans.

AbstractChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 100 leading journals. To access a ChemInform Abstract of an article which was published elsewhere, please select a “Full Text” option. The original article is trackable via the “References” option.

Absorption, transport and metabolism of carotenoids in humans

Abstract

Absorption and transport of carotenoids.

Absorption and transport of carotenoids.

Carotenoid and retinol concentrations in serum, adipose tissue and liver and carotenoid transport in sheep, goats and cattle

Carotenoid and retinol concentrations were determined in various tissues of sheep, goats and cattle, ruminants known to have widely different levels of pigmentation of their adipose tissues. An objective assessment of fat colour confirmed the whiteness of sheep and goat fat compared with that of cattle. No G-carotene was detected in the serum or fat of sheep and goats, but it was the predominant carotenoid present in the serum and fat of cattle. The major pigment present in serum and fat of sheep and goat was lutein, although its concentration was only 5-10% of that found in cattle. G-carotene was present in the liver of all three species with the highest concentration in cattle. Although lutein was the only carotenoid found in the serum and fat of sheep and goats, it could not be detected in their livers. The concentrations of retinol in serum and fat were similar for each species, but the liver of sheep had about three times the retinol concentration of the liver of goats and cattle. The transport of carotenoids in plasma was investigated. In sheep and goats, the pigments were associated mainly with very low density lipoprotein (VLDL) and low density lipoprotein (LDL), whereas in cattle, high density lipoprotein (HDL) was the major lipoprotein fraction involved.

Carotenoid transport by the larval lipophorin of the southwestern corn borer, Diatraea grandiosella

Carotenoid transport by the larval lipophorin of the southwestern corn borer, Diatraea grandiosella

Metabolism of carotenoid pigments in birds

Carotenoid pigments are an important component in the plumage of birds. The metabolic precursors are dietary in origin but many species have the capacity to chemically modify and selectively deposit the pigments. The ensuing plumage patterns are important in communication and identification. The bright yellows, oranges, and reds are due mostly to xanthophylls; keto and hydroxy carotenes. Some are deposited unmodified (e.g., lutein) whereas others are modified chemically (canthaxanthin, astaxanthin). Early workers concentrated on demonstrating that feather carotenoids were derived from the diet and deposited selectively. Progress in defining and solving biological problems depended on advances in chemical and analytical techniques. Subsequent investigation showed that various plumage colormorphs, seasonal plumage changes or colors in common mutant, were due to relatively simple chemical changes in carotenoids but had profound biological consequences. Equally important was the realization that many of these processes were under genetic control. Validation came from feeding studies of flamingos and finches. Recent studies have employed the plumage carotenoids to test hypotheses of genetic divergence, to relate plumage color to environmental process, and to demonstrate the influence of synthetic changes on color. Understanding the processes has advanced with the introduction of high-resolution separation techniques and the ability to determine both conformation and absolute configuration. The next steps will be in the direction of understanding the enzymatic modification, transport, and tissue selectivity of feather carotenoids.

Carotenoids of human colostrum

Colostrum, the initial postpartum secretion of the breast, ordinarily has a distinct yellow color due to carotenoids of its fat globules. This pigmentation progressively diminishes as milk production increases during the first week of lactation. Identity of these carotenoids was investigated by means of thin-layer chromatography, high performance liquid chromatography and spectral analysis. Alpha- and beta-carotene, lycopene and beta-cryptoxanthin were revealed as major chromogens. A component corresponding to lutein and/or zeaxanthin was also detected by both chromatographic techniques. Extracts of 23 saponified colostrum samples from 10 donors revealed considerable variation in total carotenoid concentration (0.34-7.57 micrograms/ml of colostrum). Multiparous mothers had greater mean colostrum carotenoid concentrations than did the primiparae, 2.18 +/- 1.94 vs 1.14 +/- 1.32 micrograms/ml, respectively. Seven of the eight primiparous donors' samples had little or no yellow color. These findings imply a difference in carotenoid transport by breasts that have lactated as compared to those that have not. The interrelation of carotenoids, lactation and breast cancer is discussed.

Altered Metabolism of Carotenoids During Aflatoxicosis in Young Chickens ,

Young chickens were fed from hatching until 3 weeks of age with a white corn-soy diet (containing 1.36 μg total carotenoids per gram of diet) amended with a commercial preparation of lutein, a dihydroxycarotenoid, to supply 25 μg free lutein per gram diet. The diet which also contained 0, 1, 2, 4, or 8 μg aflatoxin per gram of diet was fed to four groups of ten chickens per aflatoxin treatment until they were 3 weeks old. Aflatoxin had no effect on the partial acylation of free lutein to lutein monoester that occurs in the jejunal contents of normal birds but it decreased significantly (P<.05) the conversion of free lutein to lutein diester. Aflatoxin reduced up to 35% the lutein (94% free alcohol) content of the jejunal mucosa and the serum lutein (99% free alcohol) was reduced by up to 70%. Aflatoxin caused a slight (25%) decrease in the free lutein content of liver while increasing the monoester content 3.5-fold and the diester content 10-fold. This sequestering of lutein in the liver in esterified forms poorly transported to the integument presumably contributes to the poor pigmentation during aflatoxicosis. The forms of lutein in the toe web were diester (66%0, free alcohol (26%), and monoester (8%) and their sensitivity to aflatoxin followed the same order. These data offer clear, unequivocal proof that aflatoxin can cause poor pigmentation in birds, presumably by interfering with the absorption, transport, and deposition of carotenoids.

Studies on the absorption of beta-carotene and the distribution of total carotenoid in human serum lipoproteins after oral administration

The carotenoid increment in human serum was measured after the oral administration of aqueous dispersions and lipid dispersions of β-carotene with different test meal regimens. β-carotene was readily absorbed in both forms. Absorption of the aqueous dispersion was similar when administered with either high lipid or protein-carbohydrate test meals. Aqueous dispersions were poorly absorbed by fasting subjects. The lipoprotein distribution of the serum carotenoid increment was determined in normal, hypercholesterolemic, and hyperlipemic subjects to investigate the absorption and transport pattern for β-carotene. Peak carotenoid increments occurred first in the chylomicron and Sf 10–400 lipoprotein fractions, and considerably later in the Sf 0–10 fraction. A major part of the serum Carotenoid increment was found in the Sf 0–10 lipoprotein fraction. This is reflected in the delayed peak found in serum carotenoid tolerance curves. Very little newly absorbed carotenoid was found in the high density lipoprotein fraction. Carotenoid-to-cholesterol and carotenoid-to-fatty acid ester ratios were determined after carotenoid administration and after a lipid test meal containing no carotenoid. These ratios indicated that the peak carotenoid increments represented newly absorbed carotenoid associated with specific lipoprotein fractions rather than rapid carotenoid exchange between lipoprotein fractions that varied in their total concentration. The absorption and transport of carotenoid was compared with the absorption and transport of other lipids. Portal absorption of at least a part of the ingested carotenoid is proposed as a possible explanation for the observed carotenoid transport pattern.

The transport of carotenoids, vitamin A and cholesterol across the intestines of rats and chickens.

Research Article| April 01 1959 The transport of carotenoids, vitamin A and cholesterol across the intestines of rats and chickens J. Ganguly; J. Ganguly 1Department of Biochemistry, Indian Institute of Science, Bangalore-3, India Search for other works by this author on: This Site PubMed Google Scholar S. Krishnamurthy; S. Krishnamurthy 1Department of Biochemistry, Indian Institute of Science, Bangalore-3, India Search for other works by this author on: This Site PubMed Google Scholar S. Mahadevan S. Mahadevan 1Department of Biochemistry, Indian Institute of Science, Bangalore-3, India Search for other works by this author on: This Site PubMed Google Scholar Biochem J (1959) 71 (4): 756–762. https://doi.org/10.1042/bj0710756 Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn MailTo Cite Icon Cite Get Permissions Citation J. Ganguly, S. Krishnamurthy, S. Mahadevan; The transport of carotenoids, vitamin A and cholesterol across the intestines of rats and chickens. Biochem J 1 April 1959; 71 (4): 756–762. doi: https://doi.org/10.1042/bj0710756 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsBiochemical Journal Search Advanced Search This content is only available as a PDF. © 1959 CAMBRIDGE UNIVERSITY PRESS1959 Article PDF first page preview Close Modal You do not currently have access to this content.