Dose Of Astaxanthin Research Articles

Astaxanthin attenuates hepatic damage and mitochondrial dysfunction in non-alcoholic fatty liver disease by up-regulating the FGF21/PGC-1α pathway.

Non-alcoholic fatty liver disease (NAFLD) is considered to be one of the most common chronic liver diseases across worldwide. Astaxanthin (Ax) is a carotenoid, and beneficial effects of astaxanthin, including anti-oxidative, anti-inflammatory, and anti-tumour activity, have been identified. The present study aimed to elucidate the protective effect of astaxanthin against NAFLD and its underlying mechanism. Mice were fed either a high fat or chow diet, with or without astaxanthin, for up to 12 weeks. L02 cells were treated with free fatty acids combined with different doses of astaxanthin for 48 h. Histopathology, expression of lipid metabolism, inflammation, apoptosis, and fibrosis-related gene expression were assessed. And the function of mitochondria was also evaluated. The results indicated that astaxanthin attenuated HFD- and FFA-induced lipid accumulation and its associated oxidative stress, cell apoptosis, inflammation, and fibrosis both in vivo and in vitro. Astaxanthin up-regulated FGF21 and PGC-1α expression in damaged hepatocytes, which suggested an unrecognized mechanism of astaxanthin on ameliorating NAFLD. Astaxanthin attenuated hepatocyte damage and mitochondrial dysfunction in NAFLD by up-regulating FGF21/PGC-1α pathway. Our results suggest that astaxanthin may become a promising drug to treat or relieve NAFLD.

Effects of different levels of carotenoids and light sources on swordtail fish (Xiphophorus helleri) growth, survival rate and reproductive parameters

In this trial, the interaction between two different light resource and different levels of two pigments was investigated in order to determine their effects on growth and reproductive performance of the ornamental fish swordtail (Xiphophorus helleri) broodstock. Fish were fed with different levels of 50, 100 and 200 mg · kg-1 of astaxanthin or canthaxanthin, under two different light conditions (natural and artificial). The obtained results were more evident in animals fed with astaxanthin in comparison to canthaxanthin. Furthermore, swordtails reared under artificial light in comparison to the natural light source showed better performance. Overall the greatest effect was for the fish treated with medium dose of astaxanthin (100 mg.kg-1), under the artificial light conditions of rearing. Results indicated the important effects of all three factors (light source, dosage and carotenoids type), with significant interactions between the carotenoid dosage with carotenoid type and light source.

Effect of astaxanthin on metabolic cataract in rats with type 1 diabetes mellitus

ObjectiveThe purpose of this study was to investigate the effect of astaxanthin on metabolic cataract in rats with type 1 diabetes and its antioxidant capacity to lens. MethodsRats were randomly divided into four groups (n = 8): control group, diabetes mellitus (DM) group, low-dose astaxanthin (DM + AL) and low-dose astaxanthin (DM + AH) group. A rat model of type I diabetes mellitus was established by intraperitoneal injection of 60 mg/kg streptozotocin (STZ). After successful modeling, rats in the administration group were given different doses of astaxanthin (AST) for 12 weeks. The lens opacity of rats was observed by slit-lamp camera system. The double antibody sandwich method was used to detect the levels of advanced glycation end product (AGE), lipid peroxide/malondialdehyde (MDA), catalase (CAT), superoxide dismutase (SOD) and glutathione (GSH) in the lens. Hematoxylin-eosin (HE) staining was used to examine the morphologic changes in the lens. ResultsThe severity of cataract in the lens was obviously increased after induced by STZ, whereas it was significantly decreased after treatment with AST (p < .05, respectively). In addition, in the AST groups, the levels of AGE and MDA in the lens tissue were notably decreased when compared with those in the DM group (p < .05, respectively). However, the levels of GSH, SOD, and CAT were increased in the AST group in comparison with those in the DM group (p < .05, respectively). ConclusionsAstaxanthin may play an antioxidant role in the lens. Additionally, it exerts a protective function in the lens by delaying the development and progression of metabolic cataract and inhibiting the oxidative stress of lens in diabetic rats.

The Effect of Astaxanthin on Random Pattern Skin Flaps.

Skin flaps are the first-line treatment modality for skin defect reconstruction. With the increased importance and use of flap surgery, a growing number of studies have investigated the ways for the prevention of ischemia-reperfusion injury. The aim of this study was to investigate the effect of astaxanthin, which is an antioxidant molecule from the xanthophyll family, on the survival of random pattern skin flaps. Thirty-two Sprague-Dawley rats with a caudally based random pattern skin flap (3 × 9 cm) were divided into 4 groups: group A (astaxanthin orally 1 mg/kg per day), group B (astaxanthin orally 4 mg/kg per day), group C (astaxanthin orally 16 mg/kg per day), and the control group. On postoperative day 7, the flaps were evaluated by photographic, scintigraphic, and histological methods. Photographs were taken to investigate the total flap, necrotic flap, and surviving flap areas. A scintigraphic evaluation was undertaken to analyze the surviving area. The flaps were evaluated histopathologically for vascularization, acute inflammation, and chronic inflammation. The rate of surviving flap areas was observed to increase in parallel to the increase in the astaxanthin dose. Surviving flap areas and flap perfusion values were higher in group C compared with the control group and group A (P < 0.05). The values were also significantly higher in group B compared with control group (P < 0.05). All study groups were shown to have statistically significantly higher vascular density than the control group (P < 0.05), whereas lymphocyte and neutrophil densities were similar among all groups (P > 0.05). The photographic and scintigraphic evaluations for the viable area percentages of the flaps correlated with each other (rs = 0.913, P < 0.001). Orally administered astaxanthin, if given at doses higher than 4 mg/kg, increases flap viability rates and vascularization and can be used as an adjunctive agent.

Investigation of Astaxanthin Effect on Cisplatin Ototoxicity in Rats by Using Otoacoustic Emission, Total Antioxidant Capacity, and Histopathological Methods.

Cisplatin-induced ototoxicity is related to oxidative stress. Astaxanthin is one of the most powerful antioxidants in nature. To investigate the protective effect of astaxanthin on cisplatin-induced ototoxicity. Thirty-five Sprague Dawley female rats were divided into 5 groups: control, cisplatin, and cisplatin with 10, 20, and 40 mg/kg astaxanthin groups. Cisplatin group received a single intraperitoneal injection of 14 mg/kg cisplatin. While saline was administered in the control group, in the other 3 groups, 10, 20, and 40 mg/kg daily doses of astaxanthin were administered through orogastric cannula before administration of cisplatin. Baseline and 10th day otoacoustic emission tests were administered. An intracardiac blood sample was taken to measure total antioxidant capacity (TAC), and the cochleas of the animals were investigated histopathologically. Hearing level of astaxanthin 40 mg/kg + cisplatin group was higher at 24 kHz and 32 kHz frequencies compared to the cisplatin group. The TAC value of the cisplatin group was lower than both the control and astaxanthin + cisplatin groups (P < .05). On histopathological examination, the other groups were deformed compared to the control group, but no statistically significant difference was observed between the astaxanthin + cisplatin and cisplatin groups. Astaxanthin showed protective effect at high frequencies when it was administered at high dose. Thus, astaxanthin may have protective effect against cisplatin-induced ototoxicity.

Dietary supplementation of astaxanthin enhances hemato-biochemistry and innate immunity of Asian seabass, Lates calcarifer (Bloch, 1790)

This study aimed to evaluate the impacts of dietary astaxanthin supplementation on hematology, blood biochemistry and innate immunity of Asian seabass Lates calcarifer, with special reference to dose-response associations and variations over different phases of feeding (short-term, medium-term and long-term). Triplicate groups of fish (n = 30) with an average weight of 28 g were fed astaxanthin-incorporated diets (AX50, 50 mg kg−1 diet; AX100, 100 mg kg−1 diet; AX150, 150 mg kg−1 diet) for 90 days. A diet without astaxanthin supplement (CD) served as the control. Our findings demonstrated that fish displayed significant enhancements (P < .05) in hematological indices (white blood cell count, red blood cell count, hemoglobin and hematocrit) when fed various diets with elevated doses of astaxanthin throughout the specified phases of feeding. Serum concentrations of alanine aminotransferase (ALT), aspartate aminotransferase (AST), glucose, and cortisol in fish fed the supplemented diets decreased significantly (P < .05) with increasing dietary inclusion levels. Moreover, the provision of dietary astaxanthin at escalating doses markedly reduced (P < .05) the circulating levels of serum cholesterol (proportionately) and triglyceride (dose-dependently) in fish, following three consecutive feeding phases. Correspondingly, the supplemented fish exhibited much higher (P < .05) serum total protein content associated with astaxanthin administration. Immunological parameters (respiratory burst activity, lysozyme activity, phagocytic activity, and serum total immunoglobulin) of fish were significantly stimulated (P < .05) in response to dietary intervention with astaxanthin. The present investigation highlights the ameliorating effect of dietary astaxanthin on hemato-biochemical and immunological variables of Asian seabass and could be administered in culture protocols to improve fish immunocompetence and health.

Astaxanthin Co-Crystallized With Dark Chocolate Causes a Dose-dependent Inhibition of Oxidation Markers in Middle-aged Volunteers

Oxidative stress and antioxidant deficiency are contributing factors in aging, cardiovascular disease, diabetes and cancer. The effect of highly bioavailable polyphenols of lycosome-formulated dark chocolate (DC) containing co-crystallized astaxanthin (LF-DC-ASTX) on parameters of biological oxidation was investigated in this work. 94 healthy middle-aged volunteers (48 male, 46 female, 45 – 65 years old) were enrolled and randomized into four study groups. The 1st group were instructed to ingest conventional control DC (7.5 g). The 2nd group were asked to ingest capsules containing either 4 mg or 7 mg astaxanthin (ASTX), an algal antioxidant. The 3rd group were given DC bars (7.5 g) and 4 mg ASTX capsules for co-ingestion as two separate formulations. The 4th group were instructed to ingest LF-DC-ASTX containing different amounts of ASTX (1 mg, 2 mg, 4 mg or 7 mg) co-crystallized with 7.5 g of DC matrix. Each product was ingested once daily after breakfast for a period of 1 month. Serum levels of oxidized LDL (ox-LDL) and malonic dialdehyde (MDA) were measured after completion of 2 and 4 weeks of the study. No significant changes were observed in the values for ox-LDL or MDA concentrations in serum irrespective of cocoa content (70%, 72% or 85%) or duration of control DC intake. In contrast, ingestion of different doses of ASTX, as a single formulation, translated into reduction of oxidation markers without any dose-dependency. The inhibition of ox-LDL in volunteers following co-ingestion of DC and ASTX as two separate formulations was far greater than that seen for ASTX alone, revealing some additive effect of DC on lipid oxidation parameters. The inhibition of both oxidative markers was dose-dependent reflecting amount of ASTX in the DC matrix. These results may reflect greater bioavailability and improved pharmacokinetics for cocoa flavanols and ASTX following ingestion of LF-DC-ASTX. Therefore, nutraceutical formulations of DC fortified with ASTX can be successfully used for management of oxidative disorders associated with increased levels of ox-LDL.

Astaxanthin attenuates contrast agent-induced acute kidney injury in vitro and in vivo via the regulation of SIRT1/FOXO3a expression.

The study was processed to investigate the effect of astaxanthin (AST; 3,3-dihydroxybeta, beta-carotene-4,4-dione) on the acute kidney injury induced by iohexol and the relationship with SIRT1/FOXO3a signal pathway. Thirty male Sprague Dawley rats were randomly divided into five groups as follows: control group (CON; olive oil only), contrast media group, astaxanthin control group (100mg/kg), low astaxanthin dose group (LAG, 50mg/kg) and high astaxanthin dose group (HAG, 100mg/kg). As followed, serum creatinine (SCr), blood urea nitrogen (BUN), the oxidative stress markers and apoptosis-related proteins were detected. Human proximal tubular epithelial cells (HK-2) were cultured in DMEM/F12 medium in vitro and then randomly divided into appropriate experimental groups: normal group (N), dimethyl sulfoxide (DMSO), iohexol group (I), iohexol+(1.0, 10.0μmol/L) astaxanthin group (I+LAST; I+HAST), iohexol+SIRT1 inhibitors (nicotinamide) group (NA) and iohexol+si-RNA FOXO3a group (si-RNA FOXO3a); when cultured for 24h, cell proliferation ability was tested by cell counting kit (CCK-8), reactive oxygen species (ROS) were detected by flow cytometry and the expression of SIRT1 and FOXO3a were observed using western blot. At the end of the experiment, the levels of SCr, BUN and malondialdehyde (MDA) were all increased in the CM group. The LAG and HAG reduce superoxide anion (SOD) activity, catalase (CAT) activity, glutathione peroxidase (GPx) activity and glutathione (GSH) content, as well as SCr and BUN level. Moreover, apoptosis-associated proteins, caspase 3 p17, bax and bcl-2 were upregulated. In HK-2 cells, after adding iohexol, proliferation and intracellular ROS levels were significantly increased. Using astaxanthin in advance after the intervention, the result is opposite. SIRTl inhibitors NA can reduce the expression of SIRTl and decrease the expression of FOXO3a protein. Si-RNA FOXO3a reduces the expression of FOXO3a but had no significant effect on the expression of SIRT1. Our study demonstrates that the intervention of astaxanthin could attenuate the oxidative stress and apoptosis in contrast-induced acute kidney injury (CI-AKI), and the SIRT1/FOXO3a pathway participates in the contrast-induced apoptosis of HK-2 cells. Finally, astaxanthin reduces CI-AKI by suppression of apoptosis, which may be through inhibition of SIRT1/FOXO3a pathways.

Investigation of the effect of astaxanthin on alveolar bone loss in experimental periodontitis.

Astaxanthin is a keto-carotenoid that has a strong antioxidant effect. The purpose of this study was to evaluate the effects of astaxanthin on alveolar bone loss and histopathological changes in ligature-induced periodontitis in rats. Wistar rats were divided into four experimental groups: non-ligated (C, n=6); ligature only (L, n=6); ligature and astaxanthin (1mg/kg/day astaxanthin, AS1 group, n=8); ligature and astaxanthin (5mg/kg/day astaxanthin, AS5 group, n=8). Silk ligatures were placed at the gingival margin of lower first molars of the mandibular quadrant. The study duration was 11days and the animals were killed at the end of this period. Changes in alveolar bone levels were clinically measured and tissues were immunohistochemically examined, osteocalcin, bone morphogenic protein-2, inducible nitric oxide synthase, Bax and bcl-2 levels in alveolar bone and tartrate-resistant acid phosphatase-positive osteoclast cells, osteoblast and inflammatory cell counts were determined. Alveolar bone loss was highest in the L group and the differences among the L, AS1 and AS5 groups were also significant (P<.05). Both doses of astaxanthin decreased tartrate-resistant acid phosphatase-positive+ osteoclast cell and increased osteoblast cell counts (P<.05). The inflammation in the L group was also higher than those of the C and AS1 groups were (P<.05) indicating the anti-inflammatory effect of astaxanthin. Although inducible nitric oxide synthase, osteocalcin, bone morphogenic protein-2 and bax staining percentages were all highest in the AS5 group and bcl-2 staining percentage was highest in the AS1 group, values were close to each other (P>.05). Within the limits of this study, it can be suggested that astaxanthin administration may reduce alveolar bone loss by increasing osteoblastic activity and decrease osteoclastic activity in experimental periodontitis model.

Protective effects of astaxanthin on skin deterioration.

Astaxanthin is a carotenoid with potent antioxidant and anti-inflammatory activity. To evaluate the anti-inflammatory effect of astaxanthin on skin deterioration, we confirmed its role in epidermal-dermal interactions in vitro. Astaxanthin treatment suppressed ultraviolet B (UVB)-induced inflammatory cytokine secretion in keratinocytes, and matrix metalloproteinase-1 secretion by fibroblasts cultured in UVB-irradiated keratinocyte medium. To verify these findings, we conducted a 16-week clinical study with 65 healthy female participants. Participants were orally administered either a 6 mg or 12 mg dose of astaxanthin or a placebo. Wrinkle parameters and skin moisture content significantly worsened in the placebo group after 16 weeks. However, significant changes did not occur in the astaxanthin groups. Interleukin-1α levels in the stratum corneum significantly increased in the placebo and low-dose groups but not in the high-dose group between weeks 0 and 16. This study was performed in Japan from August to December, when changing environmental factors, such as UV and dryness, exacerbate skin deterioration. In conclusion, our study suggests that long-term prophylactic astaxanthin supplementation may inhibit age-related skin deterioration and maintain skin conditions associated with environmentally induced damage via its anti-inflammatory effect. (UMIN Clinical Trials Registry ID: UMIN000018550)

Effects of astaxanthin on blood coagulation, fibrinolysis and platelet aggregation in hyperlipidemic rats

Context: Astaxanthin (ASTX) is a xanthophyll carotenoid that reduces hemostasis in hyperlipidemic organisms. Its antihemostatic mechanisms remain unclear. Objective: The effects of ASTX on coagulation, the fibrinolytic system and platelet aggregation were investigated in hyperlipidemic rats. Materials and methods: Different doses of ASTX (5, 10 and 30 mg/kg/day, p.o.) were administered for four weeks to high-fat diet-induced hyperlipidemic rats. Serum lipid and lipoprotein levels were measured with an automatic biochemical analyzer. The prothrombin time (PT), activated partial thromboplastin time (APTT) and maximum platelet aggregation rate (MAR) were determined by a coagulation analyzer. The activities of the tissue-type plasminogen activator (t-PA), type-1 plasminogen activator inhibitor (PAI-1) and endothelial nitric oxide synthase (eNOS), as well as the levels of thromboxane B(2) [TXB(2)], 6-keto prostaglandin F(1α) [6-keto-PGF(1α)] and platelet granule membrane protein (GMP-140), were measured with enzyme-linked immunosorbent assay kits. Gene and protein expression levels were analyzed by reverse transcriptase polymerase chain reaction and Western blot, respectively. Results: ASTX (30 mg/kg) treatment in hyperlipidemic rats reduced serum TG (0.58 ± 0.14 versus 1.12 ± 0.24 mmol/L), serum TC (1.77 ± 0.22 versus 2.24 ± 0.21 mmol/L), serum LDL-C (1.13 ± 0.32 versus 2.04 ± 0.48 mmol/L), serum MDA (69%), plasma MAR (55%), serum TXB2/6-keto-PGF1α (34%) and serum GMP-140 levels (25%), plasma PAI-1 activity (48%) and downregulated the mRNA (33%) and protein (23%) expression of aorta eNOS, the mRNA (79%) and protein (72%) expression levels of aorta PAI-1. However, ASTX (30 mg/kg/d) treatment increased serum SOD activity (2.1 fold), serum GPx activity (1.8 fold), plasma PT (1.3 fold), plasma APTT (1.7 fold), serum NO (1.4-fold), serum 6-keto-PGF1α (1.3 fold). Conclusions: ASTX reduced blood coagulation and platelet aggregation and promoted fibrinolytic activity in hyperlipidemic rats. These activities were closely correlated with ASTX, maintaining the balance of t-PA/PAI-1, NO/ROS and TXA2/PGI2 in vivo.

GW26-e1009 Protective effect of astaxanthin on contrast-induced acute kidney injury in experimental rats

To explore the protective effect and mechanism of astaxanthin(AST) on the acute kidney injury induced by iohexol in rats. Thirty rats were randomly divided into five groups: control group ( CON ), iohexol group ( CM ), astaxanthin group( AST, 100mg/kg ), low astaxanthin dose group ( LAST+CM, 50mg/

Astaxanthin Induces Mitochondria-Mediated Apoptosis in Rat Hepatocellular Carcinoma CBRH-7919 Cells

We designed to study the role of mitochondria in astaxanthin-induced apoptosis in hepatocellular carcinoma cells. Effect of astaxanthin on cell proliferation was studied by using methyl thiazolyl tetrazolium (MTT) in three tumor cell lines (CBRH-7919, SHZ-88 and Lewis) and normal human hepatocyte HL-7702 cell. Cell apoptosis rate, changes of mitochondrial morphology, mitochondrial transmembrane potential and electron transport chain were evaluated respectively. Expressions of B cell lymphoma/leukemia-2 (Bcl-2) and Bcl-2 associated X protein (Bax) were detected by Western blot. Results as following, astaxanthin had little effect on HL-7702 cell, however its inhibition was most pronounced in CBRH-7919 cell line with an IC₅₀ of 39 µM. This dose of astaxanthin and CBRH-7919 cell line were chosen for further studies. Astaxanthin could induce cell apoptosis and mitochondrial membrane damage. The mitochondrial transmembrane potential and function of electron transport chain were decreased. The expression of Bcl-2 protein was down-regulated but that of Bax protein was up-regulated. In conclusion, astaxanthin showed anticancer effect by inducing cell apoptosis through the regulation of mitochondrial-dependent manner.

Retinol-deficient rats can convert a pharmacological dose of astaxanthin to retinol: antioxidant potential of astaxanthin, lutein, and β-carotene

Retinol (ROH) and provitamin-A carotenoids are recommended to treat ROH deficiency. Xanthophyll carotenoids, being potent antioxidants, can modulate health disorders. We hypothesize that nonprovitamin-A carotenoids may yield ROH and suppress lipid peroxidation under ROH deficiency. This study aimed to (i) study the possible bioconversion of astaxanthin and lutein to ROH similar to β-carotene and (ii) determine the antioxidant potential of these carotenoids with reference to Na(+)/K(+)-ATPase, antioxidant molecules, and lipid peroxidation (Lpx) induced by ROH deficiency in rats. ROH deficiency was induced in rats (n = 5 per group) by feeding a diet devoid of ROH. Retinol-deficient (RD) rats were gavaged with astaxanthin, lutein, β-carotene, or peanut oil alone (RD group) for 7 days. Results show that the RD group had lowered plasma ROH levels (0.3 µmol/L), whereas ROH rose in astaxanthin and β-carotene groups (4.9 and 5.7 µmol/L, respectively), which was supported by enhanced (69% and 70%) intestinal β-carotene 15,15'-monooxygenase activity. Astaxanthin, lutein, and β-carotene lowered Lpx by 45%, 41%, and 40% (plasma), respectively, and 59%, 64%, and 60% (liver), respectively, compared with the RD group. Lowered Na(+)/K(+)-ATPase and enhanced superoxide dismutase, catalase, and glutathione-S-transferase activities support the lowered Lpx. To conclude, this report confirms that astaxanthin is converted into β-carotene and ROH in ROH-deficient rats, and the antioxidant potential of carotenoids was in the order astaxanthin > lutein > β-carotene.

Astaxanthin uptake in domestic dogs and cats

BackgroundResearch on the uptake and transport of astaxanthin is lacking in most species. We studied the uptake of astaxanthin by plasma, lipoproteins and leukocytes in domestic dogs and cats.MethodsMature female Beagle dogs (18 to 19 mo old; 11 to 14 kg BW) were dosed orally with 0, 0.1, 0.5, 2.5, 10 or 40 mg astaxanthin and blood taken at 0, 3, 6, 9, 12, 18 and 24 h post-administration (n = 8/treatment). Similarly, mature domestic short hair cats (12 mo old; 3 to 3.5 kg body weight) were fed a single dose of 0, 0.02, 0.08, 0.4, 2, 5, or 10 mg astaxanthin and blood taken (n = 8/treatment) at the same interval.ResultsBoth dogs and cats showed similar biokinetic profiles. Maximal astaxanthin concentration in plasma was approximately 0.14 μmol/L in both species, and was observed at 6 h post-dosing. The plasma astaxanthin elimination half-life was 9 to 18 h. Astaxanthin was still detectable by 24 h in both species. In a subsequent study, dogs and cats were fed similar doses of astaxanthin daily for 15 to 16 d and astaxanthin uptake by plasma, lipoproteins, and leukocytes studied. In both species, plasma astaxanthin concentrations generally continued to increase through d 15 or 16 of supplementation. The astaxanthin was mainly associated with high density lipoprotein (HDL). In blood leukocytes, approximately half of the total astaxanthin was found in the mitochondria, with significant amounts also associated with the microsomes and nuclei.ConclusionDogs and cats absorb astaxanthin from the diet. In the blood, the astaxanthin is mainly associated with HDL, and is taken up by blood leukocytes, where it is distributed to all subcellular organelles. Certain aspects of the biokinetic uptake of astaxanthin in dogs and cats are similar to that in humans.

In vivo astaxanthin treatment partially prevents antioxidant alterations in dental pulp from alloxan‐induced diabetic rats

To evaluate the effect of astaxanthin on antioxidant parameters of dental pulp from diabetic rats. The hypothesis tested was that supplementation of diabetic rats with astaxanthin might eliminate, or at least attenuate, the defect in their antioxidative status. Wistar rats (n=32) were divided into four groups: untreated control, treated control, untreated diabetic and treated diabetic rats. A prophylactic dose of astaxanthin (20 mg kg(-1) body weight) was administered daily by gavage for 30 days. On day 23, diabetes was induced by injection of alloxan (60 mg kg(-1) body weight). After 7 days of diabetes induction, the rats were killed, and pulp tissue from incisor teeth removed. Superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx) and reductase activities were determined. Data were compared by anova and the Newman-Keuls test (P<0.05). Diabetes caused a reduction in SOD, GPx and reductase activity in dental pulp tissue. Astaxanthin had no effect on SOD and catalase activities; however, it stimulated GPx in control and diabetic rats. Diabetes altered the antioxidant system in dental pulp tissue; astaxanthin partially improved the diabetic complications.

Intraperitoneal and dietary administration of astaxanthin in rainbow trout ( Oncorhynchus mykiss) — Plasma uptake and tissue distribution of geometrical E/ Z isomers

Astaxanthin enters circulation in salmonid fishes upon intraperitoneal injection (IP) of small doses. Blood uptake and tissue distribution of geometrical E/ Z astaxanthin isomers were determined in tissues and plasma of duplicated groups of rainbow trout ( Oncorhynchus mykiss, initial weight 550 g) some of which were administered high doses of astaxanthin by IP in a trial lasting for 8 weeks. Doses of 10 (IP10), 50 (IP50) or 100 mg (IP100) astaxanthin (Lucantin Pink, BASF, Germany), respectively, dispersed in phosphate buffered saline were tested in comparison with diets containing 10 (Control) or 60 (Fed 60) mg astaxanthin kg − 1 . Astaxanthin concentrations in all examined tissues and plasma were significantly higher in IP50 and IP100 than in controls and Fed 60 ( p < 0.05). In IP50, 11 mg astaxanthin kg − 1 muscle was detected after 4 weeks, compared to 4 mg kg − 1 in rainbow trout fed 60 mg kg − 1 . Concentrations up to 80 and 100 mg astaxanthin kg − 1 were detected in liver and kidney after IP, respectively, whereas fish only fed astaxanthin contained about 2 mg astaxanthin kg − 1 . No increase in muscle astaxanthin concentration was found between 4 and 8 weeks in fish given IP, and the muscle astaxanthin concentration in IP50 and IP100 were similar. Muscle concentration and injected dose were curvilinearly correlated and the proportion of ingested dose retained by the muscle was negatively correlated with the amount of injected astaxanthin. Plasma and muscle concentrations of astaxanthin were highly correlated ( p < 0.0001). Astaxanthin Z-isomers accumulated selectively in the various tissues after IP, whereas all- E-astaxanthin was preferably absorbed into plasma when administered via the diet. There was a selective uptake of all- E-astaxanthin in the muscle of all fish. Mortality was not affected by treatment, but a dose-dependent reduction in SGR was evident after IP. In conclusion, a more rapid and higher uptake of astaxanthin in plasma, muscle, kidney and liver of rainbow trout takes place after IP compared to when astaxanthin is fed via the diet.

Tissue distribution of astaxanthin in rats following exposure to graded levels in the feed

To determine the organ distribution of high doses of astaxanthin in rats ( Rattus norvegicus) after oral application, a two week experiment was conducted, observing time (one and two weeks) and dose response (0.3, 1 and 3% of the feed). Low astaxanthin concentrations were detected in the viscera, distributed in a wide range, and not increasing from 7th to 14th day. This indicates that there was rapid elimination or catabolism and no profound long term storage. Liver concentration was unexpectedly low while the highest concentrations were found in spleen, kidneys and adrenals. The main site of astaxanthin accumulation, indeed, was the hairless skin of the tail, this was associated with red coloration (+ a ⁎ in the CIELAB tristimulus). Because the discoloration was not observed until the second week and the variability in the astaxanthin concentrations was lower, it seems that the accumulation and elimination in skin is slower, compared to other tissues. Potential adverse effects such as lesions in the kidneys of three animals and a slight (n.s.) change in the leucogram were also noted. Furthermore, astaxanthin accumulated in the eyes in the same magnitude as it is known for canthaxanthin in the eyes of rats.

Suppressive Effect of Astaxanthin Isolated from theXanthophyllomyces dendrorhousMutant on Ethanol-Induced Gastric Mucosal Injury in Rats

Ethanol has been found to induce ulcerative gastric lesion in humans. The present study investigated the in vivo protective effect of astaxanthin isolated from the Xanthophyllomyces dendrorhous mutant against ethanol-induced gastric mucosal injury in rats. The rats were treated with 80% ethanol for 3 d after pretreatment with two doses of astaxanthin (5 and 25 mg/kg of body weight respectively) for 3 d, while the control rats received only 80% ethanol for 3 d. The oral administration of astaxanthin (5 and 25 mg/kg of body weight) showed significant protection against ethanol-induced gastric lesion and inhibited elevation of the lipid peroxide level in gastric mucosa. In addition, pretreatment with astaxanthin resulted in a significant increase in the activities of radical scavenging enzymes such as superoxide dismutase, catalase, and glutathione peroxidase. A histologic examination clearly indicated that the acute gastric mucosal lesion induced by ethanol nearly disappeared after pretreatment with astaxanthin.

Effect of route of administration and carrier on bioavailability and kinetics of astaxanthin in Atlantic salmon Salmo salar L.

This study examined astaxanthin bioavailability and kinetics in adult Atlantic salmon Salmo salar L., following two different routes of astaxanthin administration (oral vs. intraperitoneal (i.p.) injection) using two different carriers of the pigment (gelatin vs. sesame oil). The dorsal aorta of adult Atlantic salmon (mean initial weight 950 g) was cannulated. The fish received a single dose of astaxanthin (572 μg kg−1) in sesame oil or (514 μg kg−1) in gelatin via the oral or i.p. route. Plasma was sampled regularly up to 72 h post oral administration and up to 510 h post i.p. injection. The astaxanthin concentration–time curves from plasma were best fit to a one-compartment pharmacokinetic model for each of the four treatments. The gelatin carrier resulted in higher availability of astaxanthin compared to the sesame oil carrier. The bioavailability for astaxanthin in sesame oil was only 38.7% of that in gelatin by i.p. injection, and only 53.5% of that in gelatin by oral administration. Higher availability of astaxanthin was observed when i.p. injection was used compared to oral administration. The bioavailability for astaxanthin administered orally was only 12% of that by i.p. injection in sesame oil, and only 8.7% of that by i.p. injection in gelatin.