Supplementing ferrets with canthaxanthin affects the tissue distributions of canthaxanthin, other carotenoids, vitamin A and vitamin E.
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To study the effects of canthaxanthin supplementation on the tissue distribution of canthaxanthin, other carotenoids, vitamin A and vitamin E, 26 spayed female ferrets (2 mo of age) were used. Ferrets were assigned to receive a commercial ferret diet and a gavage of canthaxanthin [50 mg/(kg body wt.d)] or a gavage of placebo beadlets (0 mg canthaxanthin) 5 d/wk. Serum canthaxanthin concentrations in the canthaxanthin-fed group increased from 0 at baseline to 37.76 +/- 5.34 nmol/L trans and 77.10 +/- 12.60 nmol/L cis canthaxanthin at 12 mo. Further accumulation of canthaxanthin did not occur with continuous dosing. After 2 y of receiving canthaxanthin beadlets by gavage, the ferrets did not show a detectable concentration of canthaxanthin in the eyes, nor did they have clinical signs of toxicity. Canthaxanthin concentrations were highest in liver, with high concentrations also seen in fat, lung and small intestine. The sum of alpha and beta-carotene concentrations detected in livers was significantly higher in the canthaxanthin-fed group than in the placebo-fed group, but not significantly higher when individual carotenes were compared. However, alpha-tocopherol concentrations in the livers and lungs and lutein/zeaxanthin in the fats of the ferrets fed canthaxanthin were significantly lower than in those fed the placebo. Retinoid concentrations in tissues of the ferrets fed canthaxanthin were not different from those of the placebo-fed group. The effects of canthaxanthin supplementation on other antioxidants and vitamin A nutrients demonstrate either a synergistic or antagonistic relationship, depending on the specific tissue assayed. (+info)
Chemoprevention of rat oral carcinogenesis by naturally occurring xanthophylls, astaxanthin and canthaxanthin.
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The chemopreventive effects of two xanthophylls, astaxanthin (AX) and canthaxanthin (CX) on oral carcinogenesis induced by 4-nitroquinoline 1-oxide (4-NQO) was investigated in male F344 rats. Rats were given 20 ppm of 4-NQO in their drinking water for 8 weeks to induce oral neoplasms or preneoplasms. Animals were fed diets containing 100 ppm AX or CX during the initiation or postinitiation phase of 4-NQO-induced oral carcinogenesis. The others contained the groups of rats treated with AX or CX alone and untreated. At the end of the study (week 32), the incidences of preneoplastic lesions and neoplasms in the oral cavity of rats treated with 4-NQO and AX or CX were significantly smaller than those of rats given 4-NQO alone (P < 0.001). In particular, no oral neoplasms developed in rats fed AX and CX during the 4-NQO exposure and in those given CX after the 4-NQO administration. Similarly, the incidences of oral preneoplastic lesions (hyperplasia and dysplasia) in rats treated with 4-NQO and AX or CX were significantly smaller than that of the 4-NQO-alone group (P < 0.05). In addition to such tumor inhibitory potential, dietary exposure of AX or CX decreased cell proliferation activity in the nonlesional squamous epithelium exposed to 4-NQO as revealed by measuring the silver-stained nucleolar organizer regions protein number/nucleus and 5'-bromodeoxyuridine-labeling index. Also, dietary AX and CX could reduce polyamine levels of oral mucosal tissues exposed to 4-NQO. These results indicate that AX and CX are possible chemopreventers for oral carcinogenesis, and such effects may be partly due to suppression of cell proliferation. (+info)
Cloning and expression in Escherichia coli of the gene encoding beta-C-4-oxygenase, that converts beta-carotene to the ketocarotenoid canthaxanthin in Haematococcus pluvialis.
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In the green alga Haematococcus pluvialis the ketocarotenoid astaxanthin accumulates under stress conditions. Astaxanthin is a red carotenoid pigment which possess antioxidative activity. We have cloned the gene for beta-C-4 oxygenase (beta-carotene ketolase) from the green algae H. pluvialis. The cloning method took advantage of a strain of E. coli which was genetically engineered to produce beta-carotene. An expression cDNA library of H. pluvialis was transfected to cells of this strain and visually screened for brown-red pigmented colonies. One colony out of 100,000 transformants showed color change due to accumulation of canthaxanthin. The cDNA clone in this transformant colony encodes the enzyme beta-C-4 oxygenase that catalyzes the conversion of beta carotene to canthaxanthin via echinenone. This enzyme does not convert zeaxanthin to astaxanthin. It is concluded that in H. pluvialis astaxanthin is synthesized via canthaxanthin and therefore an additional enzyme is predicted, which converts canthaxanthin to astaxanthin. (+info)
Comparative absorption and transport of five common carotenoids in preruminant calves.
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Preruminant calves, maintained in a monogastric state by feeding an all-liquid diet, were used to compare the serum appearance and lipoprotein transport of five different carotenoids over 144 h. Thirty newborn calves were fed milk replacer for 1 wk and then randomly assigned to six groups (n = 5), with each group receiving a single 20-mg oral dose of beta-carotene in water-soluble beadlets, canthaxanthin in water-soluble beadlets, lutein in oil, lycopene in oil, crystalline alpha-carotene in oil or crystalline beta-carotene in oil as part of a morning meal. Serial blood samples were taken by jugular puncture for up to 1 wk post-dosing. Lipoprotein separation and analysis were completed with selected animals. All carotenoids were absorbed, but in variable amounts. At peak serum carotenoids levels, HDL contained 70-90% of the carotenoids. Canthaxanthin and lutein peaked earlier in serum (8 and 12 h) than did the less polar lycopene, alpha-carotene, and beta-carotene (16, 24 and 24 h). Canthaxanthin and lutein were also cleared more quickly from the serum. Serum concentrations of alpha-carotene and lycopene displayed slower disappearance rates than did beta-carotene. The peak serum level (nmol/L +/- SEM) of canthaxanthin (392 +/- 136) was lower than that of beta-carotene (1245 +/- 425), and carotenoids levels of calves receiving these commercial beadlet sources were higher than the serum levels of calves receiving beta-carotene (45 +/- 17.5), alpha-carotene (42 +/- 18.0), lutein (51 +/- 9.5) and lycopene (18 +/- 4.6), which were fed in oil.(ABSTRACT TRUNCATED AT 250 WORDS) (+info)
Interactions of oral beta-carotene and canthaxanthin in ferrets.
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Interactive effects of an oral dose of equal quantities of beta-carotene and either canthaxanthin or lycopene on serum and tissue beta-carotene accumulations were investigated in domestic ferrets. Like humans, ferrets absorb a substantial portion of ingested beta-carotene intact and accumulate it in tissues. After the ferrets ingested a low carotenoid purified diet for 13 d, they were randomly assigned to one of two groups of six animals. One group was dosed with beta-carotene (10 mg/kg body weight) and the other with beta-carotene and either canthaxanthin (Experiment 1) or lycopene (Experiment 2) (10 mg/kg body weight for each). In Experiment 1, ferrets that received a combined dose of beta-carotene and canthaxanthin had serum beta-carotene concentrations that were significantly lower at 8, 12 and 24 h post-dosing (P < 0.05), compared with those that received an individual dose of beta-carotene; liver, adrenal and kidney beta-carotene concentrations were also significantly reduced. In Experiment 2, ferrets that received a combined dose of lycopene and beta-carotene had lower serum and tissue beta-carotene concentrations than in those that received beta-carotene alone; the differences were not statistically significant with the exception of serum beta-carotene concentrations at 24 h post-dosing. The results suggest that, at the doses given, a concurrent oral canthaxanthin dose has a specific antagonistic effect on the bioavailability of a beta-carotene dose in ferrets. (+info)
The carotenoids beta-carotene, canthaxanthin and zeaxanthin inhibit macrophage-mediated LDL oxidation.
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Human monocyte-macrophages were incubated for 24 h in Ham's F-10 medium with human low-density lipoprotein (LDL) in the presence or absence of beta-carotene, canthaxanthin or zeaxanthin, at final concentrations of 2.5, 12.5 and 25 mg/l. LDL oxidation, measured by agarose gel electrophoresis, the thiobarbituric acid assay and gas chromatography, was inhibited by each of the carotenoids in a concentration-dependent manner. Canthaxanthin was more effective when incorporated into LDL before addition to the cultures whereas beta-carotene and zeaxanthin were more effective when added simultaneously with LDL. The results suggest that dietary carotenoids might help slow atherosclerosis progression. (+info)
Occurrence of birefringent retinal inclusions in cynomolgus monkeys after high doses of canthaxanthin.
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PURPOSE: To reproduce and investigate in a primate animal model the phenomenon of the red carotenoid canthaxanthin (beta, beta-carotene-4'4'-dione) to induce crystal-like retinal deposits as they have been observed in the ocular fundus of humans after high canthaxanthin intake (i.e., more than 30 mg/day). METHODS: Groups of four cynomolgus monkeys (Macaca fascicularis) per gender and dose were administered 5.4, 16.2, or 48.6 mg canthaxanthin/kg body weight daily by oral gavage for 2.5 years. Eight control animals received placebo. In vivo ophthalmoscopy was performed at intervals of 3 months along with electroretinography after 12 and 24 months and retinal biomicroscopy just before the monkeys were killed. Retinal wholemounts or frozen sections were investigated postmortem by polarization, bright field, and differential interference contrast microscopy. Retinal and preterminal plasma canthaxanthin concentrations were determined by high-performance liquid chromatography (HPLC). RESULTS: By ophthalmoscopy and retinal biomicroscopy in vivo, no crystals or other light-reflecting particles were observed in the central paramacular retina. However, postmortem polarization microscopy of all 24 canthaxanthin-treated animals showed a circular zone in the peripheral retina containing birefringent, polymorphous red, orange, or white inclusions. The density of these inclusions was diminished within 1 to 8 mm posterior to the ora serrata. These inclusions were located mainly in the inner retinal layers, that is the nerve fiber layer and ganglion cell layer, inner plexiform layer, and inner nuclear layer. Twelve of the 24 canthaxanthin-treated animals showed yellow, golden birefringent inclusions in the macula. Retinas of placebo-treated monkeys were free of birefringent, crystal-like inclusions. The HPLC confirmed the presence of all-trans canthaxanthin, and 4-OH-echinenone and isozeaxanthin as well, in the retinas of all canthaxanthin-treated animals. Neither electroretinography nor histopathology indicated any adverse effects of the canthaxanthin-induced retinal inclusions seen in this study. CONCLUSIONS: A high intake of canthaxanthin for 2.5 years led to the deposition of crystal-like birefringent inclusions in the inner layers of the peripheral retina and, to some extent, the central retina of cynomolgus monkeys. The presence of these deposits did not interfere with morphology nor with retinal function. (+info)
Interactions in the postprandial appearance of beta-carotene and canthaxanthin in plasma triacylglycerol-rich lipoproteins in humans.
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We investigated the plasma appearance of beta-carotene and canthaxanthin, an oxycarotenoid, in normolipidemic premenopausal women (n = 9) who ingested beta-carotene alone, canthaxanthin alone, and a combined dose. Blood samples were taken hourly for 12 h; additional blood samples were collected over 528 h. In a subset of the women (n = 5), plasma lipoproteins were separated into chylomicrons, very-low-density-lipoproteins (VLDL) subfractions, intermediate-density lipoproteins (IDLs), and low-density lipoproteins (LDLs). The appearance of beta-carotene in plasma was biphasic, with a minor peak at 5 h followed by a sustained peak at 24-48 h. The plasma appearance of canthaxanthin was monophasic, with a rapid increase to the final hourly measurement at 12 h and a steady decrease from the next measurement at 24 h. At 6 h, 23.4 +/- 2.9% of the increase in plasma canthaxanthin was associated with LDL, in contrast with 2.4 +/- 1.4% of the increase in plasma beta-carotene (P < 0.005). Ingestion of a combined dose of beta-carotene and canthaxanthin inhibited the appearance of canthaxanthin in plasma, chylomicrons, and each VLDL subfraction (P < 0.05), but did not significantly affect the rapid accumulation of canthaxanthin in LDL within 10 h. In contrast, ingestion of the combined dose did not significantly affect the appearance of beta-carotene in plasma or plasma lipoproteins. These findings suggest distinct mechanisms of incorporation into lipoproteins and specific interactions of beta-carotene and canthaxanthin during intestinal absorption in humans. (+info)