A survey of serum and dietary carotenoids in captive wild animals. (1/44)

Accumulation of carotenoids varies greatly among animal species and is not fully characterized. Circulating carotenoid concentration data in captive wild animals are limited and may be useful for their management. Serum carotenoid concentrations and dietary intakes were surveyed and the extent of accumulation categorized for 76 species of captive wild animals at Brookfield Zoo. Blood samples were obtained opportunistically from 275 individual animals immobilized for a variety of reasons; serum was analyzed for alpha- and beta-carotene, lutein + zeaxanthin, lycopene, beta-cryptoxanthin and canthaxanthin. Total carotenoid content of diets was calculated from tables and chemical analyses of commonly consumed dietary components. Diets were categorized as low, moderate or high in carotenoid content as were total serum carotenoid concentrations. Animals were classified as unknown, high, moderate or low (non-) accumulators of dietary cartenoids. Nonaccumulators had total serum carotenoid concentrations of 0-101 nmol/L, whereas accumulators had concentrations that ranged widely, from 225 to 35,351 nmol/L. Primates were uniquely distinguished by the widest range of type and concentration of carotenoids in their sera. Most were classified as high to moderate accumulators. Felids had high accumulation of beta-carotene regardless of dietary intake, whereas a wide range of exotic birds accumulated only the xanthophylls, lutein + zeaxanthin, canthaxanthin or cryptoxanthin. The exotic ungulates, with the exception of the bovids, had negligible or nondetectable carotenoid serum concentrations despite moderate intakes. Bovids accumulated only beta-carotene despite moderately high lutein + zeaxanthin intakes. Wild captive species demonstrated a wide variety of carotenoid accumulation patterns, which could be exploited to answer remaining questions concerning carotenoid metabolism and function.  (+info)

Identification and distribution of dietary precursors of the Drosophila visual pigment chromophore: analysis of carotenoids in wild type and ninaD mutants by HPLC. (2/44)

A dietary source of retinoid or carotenoid has been shown to be necessary for the biosynthesis of functional visual pigment in flies. In the present study, the larvae or adults of Drosophila melanogaster were administered specific carotenoid-containing diets and high performance liquid chromatography was used to identify and quantify the carotenoids in extracts of wild type and ninaD visual mutant flies. When beta-carotene was fed to larvae, wild type flies were shown to hydroxylate this molecule and to accumulate zeaxanthin and a small amount of beta-cryptoxanthin. Zeaxanthin content was found to increase throughout development and was a major carotenoid peak detected in the adult fly. Carotenoids were twice as effective at mediating zeaxanthin accumulation when provided to larvae versus adults. In the ninaD mutant, zeaxanthin content was shown to be specifically and significantly altered compared to wild type, and was ineffective at mediating visual pigment synthesis when provided to both larval and adult mutant flies. It is proposed that zeaxanthin is the larval storage form for subsequent visual pigment chromophore biosynthesis during pupation, that zeaxanthin or beta-crytoxanthin is the immediate precursor for light-independent chromophore synthesis in the adult, and that the ninaD mutant is defective in this pathway.  (+info)

Carotenoid hydroxylase from Haematococcus pluvialis: cDNA sequence, regulation and functional complementation. (3/44)

A cDNA homologous to beta-carotene hydroxylase from Arabidopsis thaliana was isolated from the green alga Haematococcus pluvialis. The predicted amino acid sequence for this enzyme shows homology to the three known plant beta-carotene hydroxylases from Arabidopsis thaliana and from Capsicum annuum (38% identity) and to prokaryote carotenoid hydroxylases (32-34% identities). Heterologous complementation using E. coli strains which were genetically engineered to produce carotenoids indicated that the H. pluvialis beta-carotene hydroxylase was able to catalyse not only the conversion of beta-carotene to zeaxanthin but also the conversion of canthaxanthin to astaxanthin. Furthermore, Northern blot analysis revealed increased beta-carotene hydroxylase mRNA steady state levels after induction of astaxanthin biosynthesis. In accordance with the latter results, it is proposed that the carotenoid hydroxylase characterized in the present publication is involved in the biosynthesis of astaxanthin during cyst cell formation of H. pluvialis.  (+info)

Exogenously incorporated ketocarotenoids in large unilamellar vesicles. Protective activity against peroxidation. (4/44)

The ability of astaxanthin and canthaxanthin as chain-breaking antioxidants was studied in Cu(2+)-initiated peroxidation of phosphatidylcholine large unilamellar vesicles (LUVs). Both carotenoids increased the lag period that precedes the maximum rate of lipid peroxidation, though astaxanthin showed stronger activity. For these experiments, different amounts of xanthophylls were exogenously added to previously made LUVs, non-incorporated pigment being afterwards removed. Differential scanning calorimetry assays with L-beta,gamma-dimyristoyl-alpha-phosphatidylcholine LUVs demonstrated that xanthophylls incorporated as described interact with the lipid matrix becoming interspersed among the phospholipid molecules.  (+info)

Dose dependency of canthaxanthin crystals in monkey retina and spatial distribution of its metabolites. (5/44)

PURPOSE: To establish the threshold level of canthaxanthin crystals in the retina of cynomolgus monkeys. To correlate the spatial distribution of all-trans canthaxanthin and its metabolites with the grade of crystals. METHODS: Monkeys were orally administered 0, 0.2, 0.6, 1.8, 5.4, 16.2, and 48.6 mg/kg body wt canthaxanthin daily for 2.5 to 3 years. A second group of monkeys were administered 200 and 500 mg/kg body wt/d for 5 years. Ophthalmoscopy, electroretinography (ERG), retina and carotenoid analysis were performed as previously reported. RESULTS: Crystals in the retina periphery were observed by ophthalmoscopy preterminally only in the extreme high doses of 200 to 500 mg/kg body wt/d. There were no adverse effects on visual functions as measured by ERG. Crystals in the peripheral retina, and/or in the macula, were detected microscopically in all canthaxanthin treated groups except at the lowest dose of 0.2 mg/kg body wt/d. The grade of crystals increased up to a dose of 16.2 mg/kg body wt/d. Dose-dependent increases in canthaxanthin content also were noted in the retina, the liver, and in plasma. All-trans canthaxanthin was the major compound in the peripheral and paracentral retina of very highly dosed animals, where its concentration correlated largely with the grade of inclusions. In the macula, 4'-OH-echinenone was the dominant canthaxanthin metabolite. CONCLUSIONS: The grade of crystals in monkey retinas was dose dependent with a threshold level at 0.6 mg canthaxanthin/kg body wt/d. It correlated in the retinal periphery with the concentrations of all-trans-canthaxanthin and in the macula with its metabolites.  (+info)

Canthaxanthin supplementation alters antioxidant enzymes and iron concentration in liver of Balb/c mice. (6/44)

The 4,4'-diketo-beta-carotene, canthaxanthin, alters tocopherol status when fed to Balb/c mice, suggesting an involvement of carotenoids in the modulation of oxidative stress in vivo. We investigated further the modifications induced by an oral administration of canthaxanthin on lipid peroxidation, antioxidant enzymes and iron status in liver of Balb/c mice. Female 6-wk-old Balb/c mice were randomly divided into two groups (n = 10/group). The control group (C) received olive oil alone (vehicle) and the canthaxanthin-treated group (Cx) received canthaxanthin at a dose of 14 microg/(g body wt.d). The 15-d canthaxanthin treatment resulted in carotenoid incorporation but did not modify lipid peroxidation as measured by endogenous production of malondialdehyde (MDA). However, glutathione peroxidase activity was 35% lower (P<0.01) and catalase (59%, P<0.005) and manganese superoxide dismutase (MnSOD) (28%, P<0.05) activities were higher in canthaxanthin-treated mice than in controls. Moreover, carotenoid feeding caused a significant (P<0.05) overexpression of the MnSOD gene; mRNA levels of the enzyme were greater in treated mice than in controls. Concomitantly, a 27% (P<0.05) greater iron concentration was found in liver from canthaxanthin-treated mice compared with controls. These findings support the hypothesis that canthaxanthin alters the protective ability of tissues against oxidative stress in vivo.  (+info)

Isolation and characterization of canthaxanthin biosynthesis genes from the photosynthetic bacterium Bradyrhizobium sp. strain ORS278. (7/44)

A carotenoid biosynthesis gene cluster involved in canthaxanthin production was isolated from the photosynthetic Bradyrhizobium sp. strain ORS278. This cluster includes five genes identified as crtE, crtY, crtI, crtB, and crtW that are organized in at least two operons. The functional assignment of each open reading frame was confirmed by complementation studies.  (+info)

In vitro inhibition of proliferation of estrogen-dependent and estrogen-independent human breast cancer cells treated with carotenoids or retinoids. (8/44)

Both estrogen-receptor (ER) positive MCF-7 and ER-negative Hs578T and MDA-MB-231 human breast cancer cells were treated with carotenoids (beta-carotene, canthaxanthin and lycopene) and retinoids (all-trans-, 9-cis- and 13-cis-retinoic acid and all-trans-retinol). Among carotenoids, beta-carotene significantly reduced the growth of MCF-7 and Hs578T cells, and lycopene inhibited the growth of MCF-7 and MDA-MB-231 cells. Canthaxanthin did not affect the proliferation of any of the three cell lines. All-trans- and 9-cis-retinoic acid significantly reduced the growth of both MCF-7 and Hs578T cells, whereas 13-cis-retinoic acid and all-trans-retinol had a significant effect only on MCF-7 cells. MCF-7 and Hs578T cells treated with all-trans-retinoic acid (all-t-RA) were further studied for the mechanism behind growth inhibition. Retinoic acid receptors alpha and gamma (RARalpha, gamma) in MCF-7 cells and RARalpha, beta and gamma in Hs578T cells were not induced by all-t-RA treatment at either the protein or mRNA level. Hs578T cells treated with all-t-RA had significantly more cells in the G0/G1 stage of the cell cycle, but the same was not observed for MCF-7 cells. All-t-RA induced a dose-dependent cell death in MCF-7 cells, which may be a necrotic phenomenon. These results demonstrate that ER status is an important, although not essential factor for breast cancer cell response to carotenoid and retinoid treatments, and the mode of action of all-t-RA in MCF-7 and Hs578T cells is not through the induction of RAR. Other mechanistic pathways that are either followed by or concomitant with growth inhibition are possible.  (+info)

• 1
• 2
• 3
• 4
• 5
• 6