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PubMed1989

[Canthaxanthin retinopathy without intake of canthaxanthin].

Seven patients are described who presented with the typical fundus finding of gold-colored crystals in the superficial layers of retina in the macular area (characteristic of canthaxanthin retinopathy) without having taken canthaxanthin-containing drugs. Canthaxanthin used as a food additive is discussed as a possible cause of the crystal deposition. There may be a rather high individual tendency to develop crystal deposition, possibly related to a metabolic defect affecting canthaxanthin kinetics or to pre-existing changes in the retinal pigment epithelium. In one patient a slight decrease in crystalline deposition was observed in the course of four years.

Adult↗

PubMed1987

Canthaxanthin retinopathy. An investigation by light and electron microscopy and physicochemical analysis.

The eyes of a patient with canthaxanthin retinopathy were obtained at autopsy and examined by light and electron microscopy. Various tissues of one eye were also studied by physicochemical methods. Morphologically, there were red, birefringent, lipid-soluble crystals in the inner layers of the entire retina. They were particularly large and numerous perifoveally, where they were also clinically visible, but they also occurred frequently in a ring-shaped form peripherally and, less frequently, equatorially. The crystals were located in a spongy degeneration of the inner neuropil, where atrophy of the inner parts of the Müller cells was noticed. The compound isolated from the retina was identical with synthetic canthaxanthin according to mass and proton-resonance spectroscopy. Quantitatively, the retina contained up to 42 micrograms canthaxanthin per gram of tissue besides a minor amount of other carotenoids. Of the other tissues of the eye, only the ciliary body contained measurable concentrations of canthaxanthin. From the great number and size of the crystals, on the one hand, and the relatively small amount of isolated canthaxanthin on the other, it was concluded that the crystals presumably represent a canthaxanthin-lipoprotein complex rather than pure canthaxanthin alone. Examination showed that clinically, only the central portion of the canthaxanthin thesaurismosis, where crystals are packed most densely, can be seen.

Aged↗

PubMed1986

Canthaxanthin as a model for the study of utilization of oxycarotenoids by chickens.

A white corn-soy diet amended with varying levels (0, 5, 10, 20, 40, and 80 ppm) of canthaxanthin, a red diketocarotenoid available by chemical synthesis, and fed to young broiler chickens for 3 weeks has the attributes of a useful experimental model for the study of absorption, transport, and deposition of oxycarotenoids. On high pressure liquid chromatography of extracts of the diet and tissues of the birds, canthaxanthin predominated over the background level of nonspecific carotenoids. The concentrations of canthaxanthin found in the contents of the jejunum and large intestine and in the serum, liver, and toe web were directly proportional to the dietary concentration. Departure from such linear relationships would signal loci of action for factors affecting pigmentation. Analysis of toe webs, an integumentary depot site for carotenoids, revealed that the concentrations of canthaxanthin and two other compounds, one more polar and the other less polar than canthaxanthin, were proportional to the dietary concentration of canthaxanthin. Saponification converted the less polar compound to the more polar compound. The behavior of these compounds in response to dietary canthaxanthin, to chromatography, and to saponification can be explained by assuming that canthaxanthin, a diketocarotenoid, was partly reduced to a ketohydroxy carotenoid (hydroxyechinenone) whose hydroxyl group is acylated to form an ester. These products represent new metabolic reactions in poultry.

Animals↗

PubMed1987

Experimental carotenoid retinopathy. II. Functional and morphological alterations of the rabbit retina after acute canthaxanthin application with small unilamellar phospholipid liposomes.

Eight "chinchilla bastard" pigmented rabbits were treated intravenously with sonicated phospholipid liposomes (SUV) consisting predominantly of egg yolk phosphatidylcholine (PC). Four rabbits were treated with canthaxanthin incorporated into PC liposomes in a single injection and fractionated over a period of 19 days. The total amount of PC used was a single dose of 260 mg administered as a 50-ml suspension and 13.7 mg/fraction given as a 5-ml suspension. The total amount of canthaxanthin used was a single 40 mg as a 50-ml suspension and 2.1 mg/fraction as 5-ml suspension. Electroretinography showed that canthaxanthin produced a depression of the a-waves and prolongation of the scotopic a- and b-wave peak latencies. A single high-dose injection of PC and PC plus canthaxanthin resulted in a transitory reduction in ERG amplitudes. A single injection of PC and canthaxanthin also produced hypernormal a-waves within the recovery time. Electron microscopy demonstrated that in contrast to the controls (PC), the canthaxanthin-treated rabbits showed alterations in the RPE/photoreceptor complex, indicating that these layers are the primary site of canthaxanthin effects on the retina.

Animals↗

PubMed1987

Absorption and fate of labelled canthaxanthin 15, 15'-3H2 in rainbow trout (Salmo gairdneri Rich.).

1. Using one force fed meal, absorption of labelled canthaxanthin 15,15'-3H2 was studied by collecting blood via caudal punction at regular intervals and measuring radioactivity in various tissues and organs of rainbow trout. 2. Canthaxanthin absorption showed a large variability between individuals irrespective of their sex. A rapid increase in the radioactivity linked to canthaxanthin 15,15'-3H2 is observed in the blood followed by a slow decrease. 3. Twenty-four and 72 hours after ingestion of labelled canthaxanthin by rainbow trout, the radioactivity was widely distributed. From the total radioactivity given, most was found 24 hours after the meal in the pyloric caeca, ovary and skin. Seventy-two hours after diet, the radioactivity increased in the muscle, liver and kidney. On the other hand, the percentage of radioactivity of intestine and caeca declined. 4. Data from absorption curve indicates that 0.86% of radioactivity ingested is present in the blood, suggesting that canthaxanthin is not readily transferred from the digestive tract. 5. The metabolic clearance of canthaxanthin (lambda = 0.0246/hr +/- 0.005) which would correspond to a half-life of 28 hours gives a preliminary idea of the digestive and metabolic utilization of canthaxanthin by the rainbow trout.

Animals↗

PubMed1991

Effect of canthaxanthin on chemically induced mammary carcinogenesis.

Canthaxanthin, a carotenoid with no vitamin A activity, was evaluated for its efficacy in the prevention of chemically induced mammary cancers. Canthaxanthin was administered in the diet at two dose levels (3,390 or 1,130 mg/kg diet). In the dimethylbenzanthracene-induced mammary cancer model, diet supplementation with canthaxanthin for 3 weeks prior to the carcinogen resulted in a 65% reduction in the number of mammary cancers. The feeding of canthaxanthin after the administration of methylnitrosourea had no significant effect on mammary carcinogenesis. These data demonstrate that canthaxanthin, at least in these models of mammary cancer, is active in preventing cancer initiation and not promotion. Analysis of tissues by high-pressure liquid chromatography revealed that canthaxanthin levels in the liver are very high when compared to those in the mammary gland. The observation that canthaxanthin is highly effective in preventing cancer initiation without toxicity suggests that carotenoids not possessing vitamin A activity should be further evaluated as chemopreventive agents.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed1976

[Influence of some nutritional factors on the canthaxanthine pigmentation of the rainbow trout].

The present investigation was made to approve nutritionnal factors which affect the utilisation of food canthaxanthin by hatchery trout. Rainbow trout were obtained from a commercial trout farm, kept in running water and feeding in experimental pellets for 4 to 8 weeks. Five diets were tested (1-standard [7.5 u.i/g], 2-low protein content, 3-High lipid content, 4-non supplemented with vitamin A, 5-High vitamin A content [23 U.I./g]). All diets containing 250 mg of canthaxanthin per kilo of food, the fish were fed at the rate of approximately 2.5 p. 100 of their body weight per day. The estimation of canthaxanthin from fish tissues was accomplished as follows: the tissues were gomogeneized and extracted with several volumes of solvents. The solution containing all the pigment was evaporated. The purification of the canthaxanthin was obtained by column silica gel chromatography. The pigment was eluated with ethyl-ether as solvent. Quantitative assay of total carotenoïd was effected by spectre photometric estimation of optical density at 480 nm of this fraction dissolved in benzene. The carotenoïd composition of this fraction was studied by silica-gel thin layer chromatography. In these conditions:--it was shown by spectral studies that the canthaxanthins present in the diet are essentially those deposed in the flesh of the trout fed;--a series of experiment were made to examine the effect of composition of artificially composed feeds for pigmentation of the rainbow trout. The pigment deposition was found to correlate with the amount of lipids present in these diet. In this condition, the pigment is more dispersed with lipids present and the pigment absorption may be facilitated and later be deposed. 8 weeks alimentation are needed to observe the effect of these nutritionnal factor;--when the diet is non supplemented with vitamin A, the same quantity of canthaxanthin mixed with this food gives trout redder flesh than the standard diet. On an other hand, an antagonist effect of diet with high vitamin A content is demonstrated on the amount of the pigment deposed in the flesh of trout;--no effect of protein content of the diet was found in these experiments;--no effect of ratio calorie/protein of the diets with the intensity of deposed pigment in the flesh rainbow trout;--a correlation between neutral lipids of the tissue and the pigment deposed in the flesh of the trout fed with canthaxanthin was confirmed.

Animal Nutritional Physiological Phenomena↗

PubMed1991

Canthaxanthin and excess vitamin A alter alpha-tocopherol, carotenoid and iron status in adult rats.

beta-Carotene and excess vitamin A have been shown to reduce plasma alpha-tocopherol when fed to young rats. The present study assessed the effects of beta-carotene, excess vitamin A and canthaxanthin (4,4'-diketo-beta-carotene) on carotenoid, alpha-tocopherol and iron status in adult retired breeder rats. Male 8- to 10-mo-old rats (10/group) were fed varying levels of vitamin A as retinyl palmitate, beta-carotene and canthaxanthin ad libitum for 8 wk. The AIN-76A diet was modified to contain 16% (wt/wt) fat and 50% carbohydrate (control) plus beta-carotene or canthaxanthin at 0, 0.048 (BC1 or CX1) and 0.2% (BC2 or CX2) of the diet. These compounds were fed with and without excess retinyl palmitate (RP, 220 mg/kg). Higher relative liver weights were observed in CX- and RP-fed groups. Plasma retinyl esters were detected in all RP-fed groups. Plasma retinyl palmitate was 1.6- and 1.5-fold higher in RP-BC and RP-CX groups, respectively, than in the RP groups. Plasma and liver beta-carotene and canthaxanthin were 11-54% and 26-74% lower, respectively, with excess retinyl palmitate feeding. Feeding canthaxanthin and retinyl palmitate but not beta-carotene, resulted in lower levels of plasma alpha-tocopherol. Liver non-heme iron levels were also lower in CX-fed rats irrespective of retinyl palmitate feeding. These results extend to adult rats previous findings that excess retinyl palmitate alters vitamin E and carotenoid status prior to the manifestation of clinical signs of hypervitaminosis A. Additionally, canthaxanthin feeding lowers alpha-tocopherol and iron status in adult rats.

Administration, Oral↗

PubMed1985

Canthaxanthin.

Canthaxanthin is used as a food-coloring agent, a photoprotective agent in certain photodermatoses, a tan-simulating agent, and a pigment to darken vitiliginous skin. This article reviews the current literature on canthaxanthin and reports the evaluation of oral canthaxanthin as an artificial pigment for the management of vitiligo. Fifty-six patients were studied, using serum canthaxanthin levels, pre- and post-treatment photographs with standard conditions, physician assessment, and patient questionnaires evaluating treatment results. Canthaxanthin was rated "very satisfactory" by 10%, "satisfactory" by 35%, and "unsatisfactory" by 54% of patients. In light-skinned individuals, self-reports were "very satisfactory" in 27%, "satisfactory" in 45%, and "unsatisfactory" in 27%. In dark-skinned individuals, the treatment was less effective. Women were happier with the results than men. Major side effects were red stools and orange palms and soles. Canthaxanthin can be taken orally, is easy to use, and can be a cosmetically acceptable therapy in selected cases of vitiligo.

Adolescent↗

PubMed1991

Studies on the carotenoids in the muscle of salmon--V. Combination of astaxanthin and canthaxanthin with bovine serum albumin and egg albumin.

1. Bovine serum albumin (BSA) and/or egg albumin were bound to astaxanthin or canthaxanthin easily and the spectroscopic characteristics of these complexes were similar to those of astaxanthin or canthaxanthin in the salmon muscle. 2. This result indicates that astaxanthin-BSA, -egg albumin, canthaxanthin-BSA and -egg albumin complexes were basically similar to astaxanthin-actomyosin and/or canthaxanthin-actomyosin complex in the salmon muscle. 3. The binding of salmon actomyosin to astaxanthin or canthaxanthin is not specific.

Actomyosin↗

PubMed1992

[Canthaxanthin retinopathy. Follow-up of over 6 years].

After long-term treatment with high dosages, canthaxanthin causes a characteristic retinopathy with circular, macula surrounding crystals. As changes in retinal functionning disappear relatively easily after withdrawal of the drug, the crystals dissolve rather slowly--over about several years. Five patients showing a profound crystalline retinopathy were re-examined with an average of 69.7 months after withdrawal of the canthaxanthin-containing drug. Three of the patients were treated for erythropoetic protoporphyria (EPP) with Phenoro (2/5 beta-carotene, 3/5 canthaxanthin), two sisters took a canthaxanthin-containing formulation (1/8 beta-carotene, 7/8 canthaxanthin) for cosmetic reasons. Two female patients complained about an increased glare sensitivity, which was explainable for one of them with a subcapsular cataract. The retinal crystals decreased quite differently. Minor deffects of the retinal pigment epithelium remained unchanged in two patients. They increased slightly in the female patient with the smallest crystal formation but highest plasma cholesterol. Shortly after withdrawal of the drugs usually an increase of a-wave amplituded of the electroretinograms was found. The a-waves returned to normal and the b-wave amplitudes showed an increase up to the final control paralleling the reduction of the retinal crystals. A- and b-wave peak latencies which were prolonged under treatment returned to normal.

Adult↗

PubMed1990

Distribution of [14C]canthaxanthin and [14C]lycopene in rats and monkeys.

The absorption and distribution of [14C]-canthaxanthin and [14C]lycopene were studied in rats and in rhesus monkeys following the oral administration of [14C]canthaxanthin or [14C]lycopene in olive oil supplemented with 1 mg alpha-tocopherol/mL. For canthaxanthin and lycopene, peak accumulation of radioactivity in plasma occurred between 4 and 8 h in rats and between 8 and 48 h in monkeys. In rats, the liver contained the largest amount of both kinds of radioactive pigments. In monkeys, with the exception of one stomach sample, liver was also the major depot organ for both canthaxanthin and lycopene. The other organs tested accumulated various amounts of pigment. No labeled metabolic products of either canthaxanthin or lycopene were found.

Administration, Oral↗

PubMed1991

Reduction of murine cutaneous UVB-induced tumor-infiltrating T lymphocytes by dietary canthaxanthin.

The effect of dietary canthaxanthin, retinyl palmitate, or their combination on the tumor-infiltrating T-lymphocyte response (T-TIL) in de novo murine ultraviolet type B irradiation-induced tumors was investigated to elucidate potential mechanisms of action of these compounds. We found that dietary canthaxanthin greatly reduced the number of tumor-infiltrating helper/inducer, suppressor/cytotoxic, and interleukin-2 receptor-positive T lymphocytes and also observed a concomitant statistically significant increase in tumour incidence in canthaxanthin-fed animals. The addition of retinyl palmitate to the canthaxanthin diet ameliorated this negative effect on TIL and the development of skin tumors. We conclude that dietary retinyl palmitate and canthaxanthin can modulate the host T-cell immune response within a growing tumor and may affect tumorigenicity.

Animals↗

PubMed1989

The effects of vitamin A, beta-carotene and canthaxanthin on vitamin A metabolism and immune responses in the chick.

Chicks were fed diets containing, 0, 0.85 and 350 mg/kg vitamin A and 1 g/kg beta-carotene or canthaxanthin from hatching. Carotene increased and canthaxanthin depressed plasma and hepatic vitamin A concentrations. High vitamin A levels decreased the concentration of both carotenoids. Neither carotene nor canthaxanthin affected intestinal carotene cleavage in vitro. T-lymphocyte proliferative responses were decreased at low vitamin A intakes and enhanced at the high vitamin A intake. Carotene and canthaxanthin fed with 0.85 mg/kg vitamin A had no effect on immune response and with 350 mg/kg vitamin A prevented the enhancement of the proliferative response. It is concluded that immune response in the chick is modulated by vitamin A; carotene and canthaxanthin effects are probably due to influences on vitamin A metabolism.

Animals↗

PubMed1988

Static perimetry in canthaxanthin maculopathy.

We performed threshold static perimetry on 19 patients who had ingested canthaxanthin; 11 had maculopathy and eight did not. Patients with no history of canthaxanthin ingestion served as controls. All patients had visual acuity of 6/9 or better. Threshold static perimetry was reevaluated two to three years after cessation of canthaxanthin ingestion. For both testing sessions, patients with maculopathy presented lower retinal sensitivity than controls, while patients without maculopathy did not differ significantly from the control group. These results suggest that canthaxanthin retinopathy can adversely affect the neurosensory retina.

Adult↗

PubMed1989

Canthaxanthin retinopathy. Anatomic and functional reversibility.

Canthaxanthin intake is associated with golden yellow crystalline deposits in the retina around the macula and low static luminance threshold. Our study assesses the anatomic and functional reversibility of canthaxanthin retinopathy. The number of retinal deposits was evaluated in nine patients, two to four times over a mean period of 55 months. There was no significant difference after a nine-month follow-up. A statistically significant decrease in the number of retinal deposits was found after an observation period of 26 months. The deposits disappeared slowly, while some remained even seven years after canthaxanthin therapy was discontinued. Threshold static perimetry performed on eight patients with retinopathy and seven controls did not differ significantly between the two groups at the end of the follow-up period. The results demonstrate that canthaxanthin retinopathy is reversible.

Adult↗

PubMed1989

Reduction of immunosuppression in UV-irradiated mice by dietary retinyl palmitate plus canthaxanthin.

The ability of dietary retinyl palmitate, canthaxanthin or the combination of both, to prevent induction of immunosuppression by UVB irradiation was tested by passive transfer of splenocytes. The basal diet was the American Institute of Nutrition diet 76A, containing 4 IU retinyl palmitate/g diet. Groups of 55 mice were fed this basal diet alone, or supplemented with 120 IU retinyl palmitate/g diet, 1% canthaxanthin or the combination of both. After 18 weeks of these diets, UVB radiation treatments began. The UVB radiation source was a bank of six unfiltered Westinghouse FS40 lamps which delivered an average dose of 4.6 J/m2/s over the wavelength range of 280-340 nm. After 27.5 weeks of UV treatments, and approximately 1.14 X 10(6) J/m2, spleens were removed from mice and used as sources of splenocytes for passive transfer into naive recipients. These recipients were then challenged with an immunogenic, syngeneic UV-induced tumor (UV20). Approximately twice as many tumor challenges grew in recipients of splenocytes from UV-irradiated (19/20), as compared with unirradiated (11/20) donors fed the basal diet. Transfer of splenocytes from UV-irradiated donors fed the basal diet admixed with 1% canthaxanthin, 120 IU retinyl palmitate/g diet or the combination, resulted in 16/20, 13/20 and 10/20 growing tumors, respectively. These values were insignificantly (P = 0.25), marginally (P = 0.054) or significantly (P less than 0.02) different from the positive control value, respectively. Thus, dietary supplementation with retinyl palmitate plus canthaxanthin prevented the transfer of UV-induced immunosuppression with splenocytes from UV-irradiated mice.

Animals↗

PubMed1986

Effect of beta-carotene and canthaxanthin on the immune responses of the rat.

Male Wistar Kyoto rats were fed diets containing either 2 g/kg (0.2%) beta-carotene, canthaxanthin or basal diet for up to 66 wk. Plasma and tissues were analyzed for vitamin A, vitamin E, beta-carotene or canthaxanthin levels. In vitro immune responses of splenocytes to T- and B-lymphocyte mitogens were determined. T- and B-lymphocyte responses were consistently enhanced in the groups fed beta-carotene or canthaxanthin. Since canthaxanthin cannot be converted to vitamin A, the immunoenhancement seen in these experiments is attributed to a carotenoid effect.

Animals↗