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PubMed1992

Potent preventive action of alpha-carotene against carcinogenesis: spontaneous liver carcinogenesis and promoting stage of lung and skin carcinogenesis in mice are suppressed more effectively by alpha-carotene than by beta-carotene.

Although beta-carotene has been considered to be a key cancer preventive agent in green and yellow vegetables, other types of carotenoids, such as alpha-carotene, may also contribute to anticarcinogenic action, since these carotenoids usually coexist with beta-carotene and are detectable in human blood and tissues. In this study, we compared the inhibitory effect of natural alpha-carotene, obtained from palm oil, with that of beta-carotene on spontaneous liver carcinogenesis in C3H/He male mice. The mean number of hepatomas per mouse was significantly decreased by alpha-carotene supplementation (per os administration in drinking water at a concentration of 0.05%, ad libitum) as compared with that in the control group (P < 0.001, Student's t test). On the other hand, beta-carotene, at the same dose as alpha-carotene, did not show any such significant difference from the control group. Furthermore, we also compared the antitumor-promoting activity of alpha-carotene with that of beta-carotene against two-stage mouse lung carcinogenesis (initiator, 4-nitroquinoline 1-oxide; promoter, glycerol). alpha-Carotene, but not beta-carotene, reduced the number of lung tumors per mouse to about 30% of that in the control group (P < 0.001, Student's t test). The higher potency of the antitumor-promoting action of alpha-carotene compared to beta-carotene was confirmed in other experimental systems; e.g., alpha-carotene was also found to have a stronger effect than beta-carotene in suppressing the promoting activity of 12-O-tetradecanoylphorbol-13-acetate on skin carcinogenesis in 7,12-dimethylbenz[a]anthracene-initiated mice. These results suggest that not only beta-carotene, but also other types of carotenoids, such as alpha-carotene, may play an important role in cancer prevention.

4-Nitroquinoline-1-oxide↗
PubMed1995

Intestinal beta-carotene absorption and cleavage in men: response of beta-carotene and retinyl esters in the triglyceride-rich lipoprotein fraction after a single oral dose of beta-carotene.

Postprandial response curves of beta-carotene and retinyl esters in a triglyceride-rich lipoprotein (TRL) fraction were evaluated as a potential measure of beta-carotene uptake and cleavage. beta-Carotene, retinyl ester, and triglyceride concentrations in the TRL fraction (density < 1.006 kg/L) and plasma were measured in 10 men for 8 or 16 h after an oral dose of 15 mg beta-carotene. The beta-carotene response, unlike the triglyceride and retinyl ester response, can be evaluated in the TRL fraction but not in plasma. Intraindividual variations in the triglyceride-adjusted response of beta-carotene and retinyl palmitate in TRL fractions were 23% and 20% and interindividual variations were 42% and 36%, respectively. A low beta-carotene response was associated with a high ratio between retinyl palmitate and beta-carotene responses (r = -0.56, P = 0.013). In conclusion, the measurement of beta-carotene and retinyl esters in the TRL fraction after a dose of beta-carotene with a vitamin A-free meal may be an appropriate method to study beta-carotene uptake and cleavage.

Administration, Oral↗
PubMed1997

Concurrent liquid chromatographic separation and photodiode array detection of retinol, tocopherols, all-trans-alpha-carotene, all-trans-beta-carotene and the mono-cis isomers of beta-carotene in extracts of human plasma.

In this report we describe the development of a method for the concurrent reversed-phase high-performance liquid chromatographic separation and photodiode array detection of human plasma retinol, tocopherols and carotenes. For a single sample injection, retinol, retinyl acetate, alpha-tocopherol, gamma-tocopherol, alpha-tocopheryl acetate, all-trans-alpha-carotene and all-trans-beta-carotene, as well as the mono-cis geometrical isomers of beta-carotene were separated and detected. Analytical separations were performed at a subambient temperature (0 degree C) over a Suplex pKb-100 reversed-phase analytical column with an isocratic mobile phase of methanol-methyl tert.-butyl ether-water (80:20:5, v/v/v) at a flow-rate of 0.8 ml/min for 60 min. Standards and samples were reconstituted in ethanol, and typically, 50 microliters was injected for analysis. By HPLC, compounds of interest were clearly resolved and detectable at the picomole level.

Carotenoids↗
PubMed1983

Thermal stereoisomerization of all-(E)-beta-carotene: (Z)-beta-carotenes and electrocyclized beta-carotenes.

Thermal isomerization of synthetic all-(E)-beta-carotene yielded a multi-component mixture composed of more than sixteen (Z)-beta-carotenes and two thermo-cyclized isomers. They were separated and purified by high-performance liquid chromatography. Ten of these were characterized by spectroscopic methods as four mono-(Z)-, five di-(Z)-, and one tri-(Z)-beta-carotenes; the 7-(Z)-, 9-(Z)-, 13-(Z)-, 15-(Z)-, 9.13-(Z)-, 9.15-(Z)-, 9.13'-(Z)-, 13.15-(Z)-, 7.13'-(Z)-, and 9.9'.13-(Z)-isomers were included. Stereochemistry of six additional (Z)-isomers obtained is, as yet, unknown, though one of them might have the 9.9'-(Z)-geometry in the molecule. This is the first report on the formation and identification of the 'sterically hindered' 7-(Z)-isomers as well as the (5 leads to 10)-thermo-cyclized products in the field of alicyclic carotenoids.

Carotenoids↗
PubMed2002

The relative vitamin A value of 9-cis beta-carotene is less and that of 13-cis beta-carotene may be greater than the accepted 50% that of all-trans beta-carotene in gerbils.

The effectiveness of beta-carotene (betaC) as a vitamin A (VA) precursor may be influenced by the proportions of cis isomers of betaC consumed in the diet. Although the metabolic fates of cis isomers of betaC are poorly understood, their retinol equivalency has been assigned a value 50% that of all-trans (at) betaC. A dose-response design was used to estimate the relative VA value (VAV) of atbetaC, 9-cis (9c) betaC and 13-cis (13c) betaC in gerbils using total liver retinol as a measure of VAV. Ten groups of gerbils received a daily dose of oil with or without betaC isomer by gavage for 7 d. Nine groups (n = 5) were divided equally among the three betaC dosing treatments with each isomer provided at 141, 275 and 418 nmol/d. Total liver VA (171-259 nmol) in gerbils administered atbetaC was higher than total liver betaC (25-53 nmol). Stores of VA and betaC in livers from gerbils administered atbetaC were higher than stores of VA and betaC in livers from those given 9cbetaC or 13cbetaC. The relative VAV of cis betaC isomers was estimated by comparing slopes of dose-response lines of all three betaC isomers using atbetaC as a reference. Total liver VA and betaC increased linearly (P < 0.05) with increasing betaC intake in gerbils gavaged with all three betaC isomer oils. The relative VAV of 9cbetaC was less (38%) and 13cbetaC was more (62%) than the assigned value of 50% that of atbetaC. Thus, the proportions of cis isomers of betaC contained in a food could negatively affect the vitamin A value of the diet.

Administration, Oral↗
PubMed1998

Low and high responders to pharmacological doses of beta-carotene: proportion in the population, mechanisms involved and consequences on beta-carotene metabolism.

The aim of this study was to assess the interindividual variability of chylomicron beta-carotene response to a pharmacological load of beta-carotene in the population, to identify the mechanisms responsible for this variability, and to evaluate its consequences on beta-carotene status and metabolism. The variability, as estimated by the 3-h chylomicron beta-carotene response to 120 mg beta-carotene in 79 healthy male volunteers, was high (CV = 61%), but it was unimodal and all the subjects had detectable chylomicron beta-carotene. In 16 subjects randomly selected among the 79, the interindividual variability of the triglyceride-adjusted chylomicron (beta-carotene + retinyl palmitate) response (0-12.5 h area under the curve) was high (CV = 54%), suggesting that there is a high interindividual variability in the efficiency of intestinal absorption of beta-carotene. The chylomicron beta-carotene response was correlated (r = 0.50, P < 0.05) with the chylomicron triglyceride response. The beta-carotene status, as assessed by beta-carotene concentration in buccal mucosal cells, was correlated (r = 0.73, P < 0.05) with the triglyceride-adjusted chylomicron beta-carotene response, i.e., with the ability to respond to beta-carotene. The triglyceride-adjusted chylomicron retinyl-palmitate response was correlated (r = 0.55, P < 0.05) with the triglyceride-adjusted chylomicron beta-carotene response. Plasma all-trans retinoic acid slightly, but significantly, increased (+40%) 3 h after the beta-carotene load, but this increase was not related to the triglyceride-adjusted beta-carotene response. In conclusion, the ability to respond to beta-carotene is highly variable, but there is probably a very small proportion of true non-responders to pharmacological doses of beta-carotene in the healthy population. This variability is apparently mainly due to interindividual differences in the efficiency of intestinal absorption of beta-carotene and in chylomicron metabolism. The ability to respond to beta-carotene can affect the beta-carotene status and the provitamin A activity of beta-carotene, but it has apparently no effect on the amount of retinoic acid appearing in the plasma after the ingestion of a pharmacological dose of beta-carotene.

Administration, Oral↗
PubMed2000

Effects of high density lipoprotein containing high or low beta-carotene concentrations on progesterone production and beta-carotene uptake and depletion by bovine luteal cells.

Luteal cells were isolated from mid-luteal heifer ovaries by collagenase digestion. Cells were cultured with DMEM/Ham's F12 medium in serum pre-treated plastic culture dishes for periods of up to 11 days. As beta-carotene is almost completely insoluble in all polar solvents, it was added to cultures in either dimethyl sulphoxide (DMSO), tetrahydrofuran (THF) or as high-density lipoprotein (HDL) containing high or low beta-carotene concentrations. Medium was replaced after 24 h, thereafter medium was changed every 48 h. Treatment of cells with DMSO alone or with beta-carotene (5 micromol/l) in DMSO both resulted in significant (P<0.01) stimulation of progesterone production. beta-Carotene (5 micromol/l) in THF did not alter progesterone production but 50 micromol/l beta-carotene in THF resulted in significant inhibition (P<0.02) of progesterone production on days 3 and 7. Cultures were also supplemented with bovine HDL preparations containing equal concentrations of cholesterol (25 microg/ml) but high or low beta-carotene (12.4 or 0.44 microg/mg of cholesterol). Both HDL preparations significantly stimulated progesterone production (P<0. 001) but the high beta-carotene HDL was significantly (P<0.02) more effective than the low beta-carotene HDL. However, when given together with bovine luteinizing hormone (bLH) or dibutyryl cAMP (dbcAMP), the high beta-carotene HDL stimulated progesterone production less than did the low HDL (P<0.01). Uptake and depletion of beta-carotene by luteal cells were also examined in culture. beta-Carotene supplementation increased luteal cell beta-carotene from an initial level of 373 ng per 10(6) cells to 2030 ng per 10(6) cells by day 6. In contrast, the levels in control cells decreased to 14% of starting values during the same period. Cells treated with HDL containing high beta-carotene on day 1 or days 1 and 3 were then incubated with or without bLH or dbcAMP for a further 2 days to investigate the effect of bLH and dbcAMP on depletion of beta-carotene by luteal cells. beta-Carotene depletion in the luteal cells was significantly higher (P<0.05) in LH- and dbcAMP-treated cells than in the control cells in both groups. These results indicate that the use of solvents such as DMSO or THF may have undesirable effects due to alteration of cell membrane permeability. Supplementation with bLH or dbcAMP may increase the metabolism of beta-carotene in luteal cells. bLH or dbcAMP together with high beta-carotene HDL may, when combined with the effect of increased beta-carotene metabolism, give less stimulation than with low beta-carotene HDL.

Animals↗
PubMed1991

Enzymatic conversion of beta-carotene into beta-apo-carotenals and retinoids by human, monkey, ferret, and rat tissues.

Whether the conversion of beta-carotene into retinoids involves an enzymatic excentric cleavage mechanism was examined in vitro with homogenates prepared from human, monkey, ferret, and rat tissue. Using high-performance liquid chromatography, significant amounts of beta-apo-12'-, -10'-, and -8'-carotenals, retinal, and retinoic acid were found after incubation of intestinal homogenates of the four different species with beta-carotene in the presence of NAD+ and dithiothreitol. No beta-apo-carotenals or retinoids were detected in control incubations done without tissue homogenates. The production of beta-apo-carotenals was linear for 30 min and up to tissue protein concentrations of 1.5 mg/ml. The rate of formation of beta-apo-carotenals from 2 microM beta-carotene was about 7- to 14-fold higher than the rate of retinoid formation in intestinal homogenates, and the rate of beta-apo-carotenal production was fivefold greater in primate intestine vs rat or ferret intestine (P less than 0.05). The amounts of beta-apo-carotenals and retinoids formed were markedly reduced when NAD+ was replaced by NADH, or when dithiothreitol and cofactors were deleted from the incubation mixture. Both beta-apo-carotenal and retinoid production from beta-carotene were inhibited completely by adding disulfiram, an inhibitor of sulfhydryl-containing enzymes. Incubation of beta-carotene with liver, kidney, lung, and fat homogenates from each species also resulted in the appearance of beta-apo-carotenals and retinoids. The identification of three unknown compounds which might be excentric cleavage products is ongoing. These data support the existence of an excentric cleavage mechanism for beta-carotene conversion.

Animals↗
PubMed1997

beta-Carotene in breast milk and serum is increased after a single beta-carotene dose.

Normal lactating mothers were administered a single dose of 60 or 210 mg beta-carotene and changes in serum and milk retinol, alpha-tocopherol, and carotenoids were monitored for 8 d. Average serum beta-carotene concentrations increased 4.1- and 4.0-fold after the 60- and 210-mg doses, respectively. Milk beta-carotene concentrations increased 4.1- and 3.0-fold after the 60- and 210-mg doses, respectively. Maximum serum concentrations were reached 24 h after both supplements, although concentrations of milk beta-carotene continued to rise for 2-3 d. After 8 d, both serum and milk beta-carotene continued to rise for 2-3 d. After 8 d, both serum and milk beta-carotene concentrations remained about twofold higher than baseline concentrations. Increases in serum or milk beta-carotene concentrations were not dose-dependent. Initial serum and milk concentrations of beta-carotene predicted increases after supplementation, and increases in serum beta-carotene concentrations predicted those in milk. Concentrations of milk carotenoids were less than one-tenth their respective concentrations in serum. Lutein, beta-cryptoxanthin, lycopene, alpha-carotene, retinol, and alpha-tocopherol concentrations in serum or milk did not change significantly after beta-carotene supplementation. Retinol esters account for most of the retinol equivalents in the milk of well-nourished mothers. Initial and maximum concentrations of beta-carotene in serum and milk were strongly correlated for individual mothers. Collectively, the data showed that a single 60-mg supplement of beta-carotene sustained elevated beta-carotene concentrations in serum and milk for > 1 wk in normal mothers but did not affect concentrations of other major carotenoids, retinol, or alpha-tocopherol.

Adult↗
PubMed1998

Effect of simultaneous, single oral doses of beta-carotene with lutein or lycopene on the beta-carotene and retinyl ester responses in the triacylglycerol-rich lipoprotein fraction of men.

The effects of lutein and lycopene on beta-carotene absorption and cleavage were investigated in 12 male subjects. Responses of carotenoids and retinyl palmitate in the triacylglycerol-rich lipoprotein (TRL) fraction after a separate 15-mg beta-carotene dose were compared with those after a dose of 15 mg beta-carotene combined with 15 mg lycopene or lutein (given as natural concentrates or extracts). After combined dosing with lutein, the areas under the curve (AUCs) of beta-carotene and retinyl palmitate in the TRL fraction, adjusted for the triacylglycerol response, were 66% (P = 0.019) and 74% (P < 0.059), respectively, compared with 100% after dosing with beta-carotene alone. After combined dosing with lycopene these percentages were 90% and 101%, respectively (NS). Beta-carotene conversion, estimated from the ratio between the AUC for retinyl esters and beta-carotene, assuming eccentric cleavage, was 69%, 71%, and 72% for treatment with only beta-carotene, beta-carotene combined with lycopene, and beta-carotene combined with lutein, respectively. In addition, a pilot study was performed to evaluate application of TRL response curves to measure absorption of carotenoids from vegetable sources (15 mg carotenoid as carrots, spinach, and tomato paste). As compared with the carotenoid concentrates, responses were considerably lower or hardly measurable (beta-carotene and retinyl palmitate after carrots, lutein after spinach), except for lycopene and retinyl palmitate after a single dose of tomato paste. In conclusion, this study showed that lutein, but not lycopene, negatively affected beta-carotene absorption when given simultaneously with beta-carotene but apparently had no effect on beta-carotene cleavage.

Absorption↗
PubMed1995

Simultaneous dietary supplementation of sodium cholate and beta-carotene markedly enhances accumulation of beta-carotene in mice.

This study evaluated whether simultaneous supplementation of sodium cholate and beta-carotene to a diet enhanced the accumulation of beta-carotene in mice. For 2 wk, male ICR mice were fed either a basal diet or a diet containing Dunaliella-bardawil beta-carotene 50 mg/100g that was or was not supplemented with sodium cholate (0.25 g/100 g). The concentrations of beta-carotene in liver and plasma were approximately 5 and 10 times higher, respectively. In the mice fed the beta-carotene diet with sodium cholate than in those fed the beta-carotene diet without sodium cholate. Beta-carotene was not detectable in the liver or plasma of mice fed either basal diet. The concentrations of vitamin E in the plasma and liver of mice fed either beta-carotene diet or the basal diet with sodium cholate were significantly lower than in those fed the basal diet. In a second study, mice were fed a diet containing 50 mg/100 g synthetic beta-carotene supplemented with various concentrations of sodium cholate (0, 0.05, 0.1, 0.25, 0.5 g/100 g) for 2 wk. The concentrations of beta-carotene and vitamin E in plasma, liver and bone marrow cells were higher in mice fed the beta-carotene diet supplemented with 0.05 g/100 g of sodium cholate than in those fed the unsupplemented diet. These findings show that simultaneous supplementation of sodium cholate and beta-carotene to a diet markedly enhances the accumulation of beta-carotene. This dietary protocol may be useful to introduce a high amount of beta-carotene in the tissue of mice in a short period of time.

Animals↗
PubMed1998

Chylomicron beta-carotene and retinyl palmitate responses are dramatically diminished when men ingest beta-carotene with medium-chain rather than long-chain triglycerides.

The effect of the ingestion of beta-carotene with medium-chain triglycerides (MCT) or long-chain triglycerides (LCT) on the bioavailability and the provitamin A activity of beta-carotene was investigated in humans. Sixteen healthy young men ingested, on two different days, a test meal containing 120 mg beta-carotene incorporated into 40 g LCT (LCT meal) or 40 g MCT (MCT meal). This meal was followed 6 h later by a beta-carotene-free meal containing 40 g LCT. Chylomicron beta-carotene, retinyl palmitate and triglycerides were measured every hour for 12.5 h after the first meal. No significant increase in chylomicron triglycerides was detected for the 6 h after the MCT meal intake, whereas a significant increase in chylomicron triglycerides was observed after the LCT meal intake. The chylomicron beta-carotene and retinyl palmitate responses to the MCT meal (0-6 h area under the curves, AUC) were significantly (P < 0.05) lower [AUC = 68.1 +/- 26.8 and 43. 4 +/- 10.4 nmol/(L.h), for beta-carotene and retinyl palmitate, respectively] than those obtained after the LCT meal [301.4 +/- 64.0 and 166.0 +/- 29.0 nmol/(L.h), respectively]. The chylomicron beta-carotene and retinyl palmitate responses obtained after the beta-carotene-free meal (6-12.5 h AUC) were also significantly lower when the first meal provided MCT rather than LCT. The chylomicron (retinyl palmitate/beta-carotene) ratios were constant during the postprandial periods, whatever the meal ingested. We conclude that the chylomicron beta-carotene response is markedly diminished when beta-carotene is absorbed with MCT instead of LCT. This phenomenon is apparently due to the lack of secretion of chylomicrons in response to MCT; however, a lower intestinal absorption of beta-carotene or a higher transport of beta-carotene via the portal way in the presence of MCT cannot be ruled out. Finally, the data obtained show that MCT do not affect the rate of intestinal conversion of beta-carotene into vitamin A.

Adult↗
PubMed1996

Alpha-Tocopherol and beta-carotene supplements and lung cancer incidence in the alpha-tocopherol, beta-carotene cancer prevention study: effects of base-line characteristics and study compliance.

BACKGROUND: Experimental and epidemiologic investigations suggest that alpha-tocopherol (the most prevalent chemical form of vitamin E found in vegetable oils, seeds, grains, nuts, and other foods) and beta-carotene (a plant pigment and major precursor of vitamin A found in many yellow, orange, and dark-green, leafy vegetables and some fruit) might reduce the risk of cancer, particularly lung cancer. The initial findings of the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study (ATBC Study) indicated, however, that lung cancer incidence was increased among participants who received beta-carotene as a supplement. Similar results were recently reported by the Beta-Carotene and Retinol Efficacy Trial (CARET), which tested a combination of beta-carotene and vitamin A. PURPOSE: We examined the effects of alpha-tocopherol and beta-carotene supplementation on the incidence of lung cancer across subgroups of participants in the ATBC Study defined by base-line characteristics (e.g., age, number of cigarettes smoked, dietary or serum vitamin status, and alcohol consumption), by study compliance, and in relation to clinical factors, such as disease stage and histologic type. Our primary purpose was to determine whether the pattern of intervention effects across subgroups could facilitate further interpretation of the main ATBC Study results and shed light on potential mechanisms of action and relevance to other populations. METHODS: A total of 29,133 men aged 50-69 years who smoked five or more cigarettes daily were randomly assigned to receive alpha-tocopherol (50 mg), beta-carotene (20 mg), alpha-tocopherol and beta-carotene, or a placebo daily for 5-8 years (median, 6.1 years). Data regarding smoking and other risk factors for lung cancer and dietary factors were obtained at study entry, along with measurements of serum levels of alpha-tocopherol and beta-carotene. Incident cases of lung cancer (n = 894) were identified through the Finnish Cancer Registry and death certificates. Each lung cancer diagnosis was independently confirmed, and histology or cytology was available for 94% of the cases. Intervention effects were evaluated by use of survival analysis and proportional hazards models. All P values were derived from two-sided statistical tests. RESULTS: No overall effect was observed for lung cancer from alpha-tocopherol supplementation (relative risk [RR] = 0.99; 95% confidence interval [CI] = 0.87-1.13; P = .86, logrank test). beta-Carotene supplementation was associated with increased lung cancer risk (RR = 1.16; 95% CI = 1.02-1.33; P = .02, logrank test). The beta-carotene effect appeared stronger, but not substantially different, in participants who smoked at least 20 cigarettes daily (RR = 1.25; 95% CI = 1.07-1.46) compared with those who smoked five to 19 cigarettes daily (RR = 0.97; 95% CI = 0.76-1.23) and in those with a higher alcohol intake (> or = 11 g of ethanol/day [just under one drink per day]; RR = 1.35; 95% CI = 1.01-1.81) compared with those with a lower intake (RR = 1.03; 95% CI = 0.85-1.24). CONCLUSIONS: Supplementation with alpha-tocopherol or beta-carotene does not prevent lung cancer in older men who smoke. beta-Carotene supplementation at pharmacologic levels may modestly increase lung cancer incidence in cigarette smokers, and this effect may be associated with heavier smoking and higher alcohol intake. IMPLICATIONS: While the most direct way to reduce lung cancer risk is not to smoke tobacco, smokers should avoid high-dose beta-carotene supplementation.

Age Factors↗
PubMed1997

Effects of supplemental beta-carotene, cigarette smoking, and alcohol consumption on serum carotenoids in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study.

We determined whether serum carotenoid or retinol concentrations were altered by beta-carotene supplementation in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study and whether such effects were modified by alcohol consumption or cigarette use. Participants in this substudy were 491 randomly selected men aged 58-76 y from the metropolitan Helsinki study center [237 receiving supplemental beta-carotene (20 mg/d) and 254 not receiving such supplementation]. Dietary carotenoids, retinol, and alcohol, and serum beta-carotene, alpha-tocopherol, retinol, and cholesterol were assessed at baseline. After an average of 6.7 y of supplementation, serum was collected and carotenoid, retinol, and alpha-tocopherol concentrations were determined by HPLC. Serum carotenoid fractions were highly correlated with each other (P < or = 0.0001). Compared with the unsupplemented group, the beta-carotene group had significantly higher serum concentrations of beta-carotene (1483%), alpha-carotene (145%), and beta-cryptoxanthin (67%) (P < or = 0.0001). Retinol concentrations were 6% higher (P = 0.03) and lutein was 11% lower (P = 0.02) in the supplemented group. Serum lycopene, zeaxanthin, and alpha-tocopherol did not differ according to beta-carotene-supplementation status. Although these beta-carotene-group differences were not significantly altered by amount of alcohol consumption, higher consumption (> 12.9 g/d, median) was related to lower (10-38%) concentrations of carotenoids, particularly beta-carotene, alpha-carotene, and beta-cryptoxanthin, in both the supplemented and unsupplemented groups. Smoking status did not significantly influence the supplementation-related differences in serum carotenoid and retinol values but concentrations of carotenoids were generally highest in participants who quit smoking while in the study and lowest in current smokers of > or = 20 cigarettes/d. This study showed that serum concentrations of non-beta-carotene carotenoids are altered by long-term beta-carotene supplementation and confirms the adverse effects of alcohol and cigarette smoking on serum carotenoids.

Aged↗
PubMed2002

Modulation of absorption of beta-carotene and tissue accumulation of beta-carotene and vitamin A by different surfactants in rats.

BACKGROUND/AIMS: The absorption of beta-carotene is closely associated with the absorption of dietary fats in the duodenum. Aim of the study was to evaluate two different surfactants, taurocholate and Pluronic L-81, which are known to stimulate or inhibit the absorption of dietary fats, respectively with regard to the absorption of beta-carotene and tissue accumulation of beta-carotene and vitamin A. METHODS: Rats were kept on a vitamin-A- deficient diet for 4 weeks and then either kept on this diet or fed this diet enriched with beta-carotene (200 mg/kg feed) alone or in combination with taurocholate (10 g/kg) or Pluronic L-81 (5 ml/kg) for another two weeks. RESULTS: beta-carotene was not detectable in liver or plasma of rats fed the deficient diet. The supplementation of beta-carotene alone led to an increase of beta-carotene in plasma and organs (p < 0.05) and resulted in an increase of vitamin A in the liver (p < 0.01), indicating its conversion. The addition of taurocholate enhanced the absorption of beta-carotene (p < 0.01), but had little affect on the levels of total vitamin A in the liver. In contrast, Pluronic L-81 caused a reduced uptake of beta-carotene as indicated by lower concentrations in plasma and liver (p < 0.01) as well as reduced total vitamin A levels in the liver (p < 0.01) either caused by the reduced availability of beta-carotene or a reduced conversion into vitamin A. CONCLUSIONS: The study shows that surfactants can modulate beta-carotene absorption differently. The results for taurocholate confirm known observations concerning an enhanced absorption of beta-carotene. Pluronic L-81 might diminish the uptake of beta-carotene into the enterocyte, which would be in disagreement with regard to its function in the absorption of total lipids in general, or might effect the excretion into the blood by modulation chylomicron secretion.

Absorption↗
PubMed1993

Cellular levels of all-trans-beta-carotene under the influence of 9-cis-beta-carotene in FU-5 rat hepatoma cells.

After incubation of FU-5 hepatoma cells for 46.5 h with synthetic all-trans-beta-carotene (3.5 microM) dissolved in tetrahydrofuran, the beta-carotene level in the cells amounted to 0.24 nmol/mg protein. No interconversion from all-trans to cis isomers occurred during incubation. Upon incubation with 3.5 microM synthetic 9-cis-beta-carotene, only 0.03 nmol 9-cis-beta-carotene/mg protein was detected in the cells. With a mixture of synthetic all-trans- (3.5 microM) and 9-cis-beta-carotene (1.0 microM), 0.09 nmol all-trans- and 0.02 nmol 9-cis-beta-carotene/mg protein were incorporated into the cells. These data suggest that 9-cis-beta-carotene and/or its decomposition products inhibited the uptake or influenced the metabolism of all-trans-beta-carotene. Thus, the lack of an increase in human serum levels of 9-cis-beta-carotene upon intake of a mixture of all-trans- and cis-beta-carotene isomers dissolved in soybean oil, Betatene (Stahl et al. (1993) J. Nutr. 123, 847-851), may be due to particular biokinetic or metabolic parameters for cis isomers of beta-carotene as compared to all-trans-beta-carotene.

Animals↗
PubMed1993

Preferential inhibition of LDL oxidation by the all-trans isomer of beta-carotene in comparison with 9-cis beta-carotene.

The synthetic all-trans isomer of beta-carotene was recently shown to possess antioxidant properties towards the formation of oxidized low density lipoprotein. In the present study, the binding of the all-trans and the 9-cis isomers of beta-carotene to plasma lipoproteins was investigated, and the effect of these isomers on the susceptibility of plasma lipoprotein to lipid peroxidation and on macrophage uptake of oxidized LDL were studied. Both the synthetic all-trans isomer of beta-carotene and the natural beta-carotene from the algae Dunaliella Bardawil [which is composed of the all-trans (70%) and the 9-cis (30%) isomers], were found to bind similarly to all plasma lipoproteins, following the incubation of beta-carotene with purified lipoproteins or with whole plasma. Incubation of the beta-carotene isomers with whole plasma, followed by separation of the lipoproteins, revealed substantial carotene binding to very low density lipoprotein (VLDL) and to LDL and limited binding to high density lipoprotein (HDL). Lipid peroxidation of VLDL and LDL were significantly inhibited by beta-carotene. The synthetic beta-carotene, however, was twice as effective as the Dunaliella beta-carotene in inhibiting LDL lipid peroxidation (following LDL incubation with copper ions). Cellular degradation of oxidized lipoproteins (mediated via the scavenger receptor) was decreased by 40% and 18%, respectively, when they were prepared by incubation in the presence of synthetic or natural beta-carotene; the control oxidized LDL was prepared in the absence of beta-carotene.(ABSTRACT TRUNCATED AT 250 WORDS)

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