Astaxanthin Abstracts 3

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Building strength, endurance, and mobility using an astaxanthin formulation with functional training in elderly.
            (Liu et al., 2018)  Download
BACKGROUND:  Building both strength and endurance has been a challenge in exercise training in the elderly, but dietary supplements hold promise as agents for improving muscle adaptation. Here, we test a formulation of natural products (AX: astaxanthin, 12 mg and tocotrienol, 10 mg and zinc, 6 mg) with both anti-inflammatory and antioxidant properties in combination with exercise. We conducted a randomized, double-blind, placebo-controlled study of elderly subjects (65-82 years) on a daily oral dose with interval walking exercise on an incline treadmill. METHODS:  Forty-two subjects were fed AX or placebo for 4 months and trained 3 months (3×/week for 40-60 min) with increasing intervals of incline walking. Strength was measured as maximal voluntary force (MVC) in ankle dorsiflexion exercise, and tibialis anterior muscle size (cross-sectional area, CSA) was determined from magnetic resonance imaging. RESULTS:  Greater endurance (exercise time in incline walking, >50%) and distance in 6 min walk (>8%) accompanied training in both treatments. Increases in MVC by 14.4% (±6.2%, mean ± SEM, P < 0.02, paired t-test), CSA by 2.7% (±1.0%, P < 0.01), and specific force by 11.6% (MVC/CSA, ±6.0%, P = 0.05) were found with AX treatment, but no change was evident in these properties with placebo treatment (MVC, 2.9% ± 5.6%; CSA, 0.6% ± 1.2%; MVC/CSA, 2.4 ± 5.7%; P > 0.6 for all). CONCLUSIONS:  The AX formulation improved muscle strength and CSA in healthy elderly in addition to the elevation in endurance and walking distance found with exercise training alone. Thus, the AX formulation in combination with a functional training programme uniquely improved muscle strength, endurance, and mobility in the elderly.

Dietary Supplementation with Astaxanthin-Rich Algal Meal Improves Strength Endurance–A Double Blind Placebo Controlled Study on Male Students
            (Malmsten and Lignell, 2008)  Download
The present study was designed to investigate the effect of dietary supplementation with astaxanthin on physical performance. Forty healthy paramedic students were recruited for this test in a double blind placebo controlled study. In this study, we used algal meal (AstaREAL® biomass) as astaxanthin supplementation. Twenty of the subjects received capsules filled with algal meal to provide 4 mg astaxanthin per capsule, whereas the other twenty received placebo capsules for six months. The physical parameters monitored were fitness, strength/endurance and strength/explosivity by standardized exercises. Before starting the dietary supplementation, base values for each of the subjects were obtained. At the end of the six month period of dietary supplementation, the average number of knee bendings (squats) increased by 27.05 (from 49.32 to 76.37) for subjects having received astaxanthin and by 9.0 (from 46.06 to 55.06) for the placebo subjects. Hence, the increase in the astaxanthin supplemented group was three times higher than that of the placebo group (P=0.047). None of the other parameters monitored differed significantly between the groups at the end of the study period. Based on this findings, it suggested that supplementation of astaxanthin is effective for the improvement of strength endurance that may lead to sports performance.

Astaxanthin protects mesangial cells from hyperglycemia-induced oxidative signaling.
            (Manabe et al., 2008)  Download
Astaxanthin (ASX) is a carotenoid that has potent protective effects on diabetic nephropathy in mice model of type 2 diabetes. In this study, we investigated the protective mechanism of ASX on the progression of diabetic nephropathy using an in vitro model of hyperglycemia, focusing on mesangial cells. Normal human mesangial cells (NHMCs) were cultured in the medium containing normal (5 mM) or high (25 mM) concentrations of D-glucose. Reactive oxygen species (ROS) production, the activation of nuclear transcription factors such as nuclear factor kappa B (NFkappaB) and activator protein-1 (AP-1), and the expression/production of transforming growth factor-beta 1 (TGFbeta(1)) and monocyte chemoattractant protein-1 (MCP-1) were evaluated in the presence or absence of ASX. High glucose (HG) exposure induced significant ROS production in mitochondria of NHMCs, which resulted in the activation of transcription factors, and subsequent expression/production of cytokines that plays an important role in the mesangial expansion, an important event in the pathogenesis of diabetic nephropathy. ASX significantly suppressed HG-induced ROS production, the activation of transcription factors, and cytokine expression/production by NHMCs. In addition, ASX accumulated in the mitochondria of NHMCs and reduced the production of ROS-modified proteins in mitochondria. ASX may prevent the progression of diabetic nephropathy mainly through ROS scavenging effect in mitochondria of mesangial cells and thus is expected to be very useful for the prevention of diabetic nephropathy.

Effects of astaxanthin on human blood rheology.
            (Miyawaki et al., 2008)  Download
Effects of astaxanthin (AX) derived from H. pluvialis on human blood rheology were investigated in 20 adult men with a single-blind method. The experimental group was 57.5 +/- 9.8 years of age and the placebo group was 50.8 +/- 13.1 years of age. A blood rheology test that measures whole blood transit time was conducted using heparinized blood of the volunteers by a MC-FAN apparatus (microchannel array flow analyzer). After administration of AX 6 mg/day for 10 days, the values of the experimental group were decreased from 52.8 +/- 4.9 s to 47.6 +/- 4.2 s (p<0.01) and a comparison of the values between the experimental (47.6 +/- 4.2 s) and the placebo (54.2 +/- 6.7 s) groups showed a significant difference (p<0.05). There were no adverse effects resulting from the administration of AX 6 mg/day for 10 days. Informed consent was obtained from each subject.

Astaxanthin inhibits tumor invasion by decreasing extracellular matrix production and induces apoptosis in experimental rat colon carcinogenesis by modulating the expressions of ERK-2, NFkB and COX-2.
            (Nagendraprabhu and Sudhandiran, 2011)  Download
Colon cancer is the third most malignant neoplasm in the world and it remains an important cause of mortality in Asian and Western countries. Astaxanthin (AST), a major component of carotenoids possesses attractive remedial features. The purpose of this study is to investigate the possible mechanism of action of astaxanthin against 1, 2 dimethyl hydrazine (DMH)-induced rat colon carcinogenesis. Wistar male rats were randomized into five groups, group 1 were control rats, group 2 were rats that received AST (15 mg/kg body wt p.o. everyday), rats in group 3 were induced with DMH (40 mg/kg body wt, s.c.), DMH-induced rats in groups 4 and 5 were either pre or post initiated with AST, respectively as in group 2. DMH-induced rats exhibited elevated expressions of Nuclear factor kappa B-p65 (NF-κB-p65), Cyclooxygenase-2 (COX-2), Matrixmetallo proteinases (MMP) 2/9, Proliferating cell nuclear antigen (PCNA), and Extracellular signal-regulated kinase-2 (ERK-2) as confirmed by immunofluorescence. Further, Westernblot analysis of MMPs-2/9, ERK-2 and Protein kinase B (Akt) revealed increased expressions of these proteins in DMH-induced groups of rats. AST-treatment decreased the expressions of all these vital proteins, involved in colon carcinogenesis. The ability of AST to induce apoptosis in the colon of DMH-induced rats was confirmed by Annexin-V/PI staining in a confocal microscopy, DNA fragmentation analysis and expression of caspase-3 by Western blotting. In conclusion, astaxanthin exhibits anti-inflammatory and anti-cancer effects by inducing apoptosis in DMH-induced rat colon carcinogenesis by modulating the expressions of NFkB, COX-2, MMPs-2/9, Akt and ERK-2.


 

Prevention of diabetic nephropathy by treatment with astaxanthin in diabetic db/db mice.
            (Naito et al., 2004)  Download
Oxidative stress is implicated as an important mechanism by which diabetes causes nephropathy. Astaxanthin, which is found as a common pigment in algae, fish, and birds, is a carotenoid with significant potential for antioxidative activity. In this study, we examined whether chronic administration of astaxanthin could prevent the progression of diabetic nephropathy induced by oxidative stress in mice. We used female db/db mice, a rodent model of type 2 diabetes, and their non-diabetic db/m littermates. The mice were divided into three groups as follows: non-diabetic db/m, diabetic db/db, and diabetic db/db treated with astaxanthin. Blood glucose level, body weight, urinary albumin, and urinary 8-hydroxydeoxyguanosine (8-OHdG) were measured during the experiments. Histological and 8-OHdG immunohistochemical studies were performed for 12 weeks from the beginning of treatment. After 12 weeks of treatment, the astaxanthin-treated group showed a lower level of blood glucose compared with the non-treated db/db group; however, both groups had a significantly high level compared with the db/m mice. The relative mesangial area calculated by the mesangial area/total glomerular area ratio was significantly ameliorated in the astaxanthin-treated group compared with the non-treated db/db group. The increases in urinary albumin and 8-OHdG at 12 weeks of treatment were significantly inhibited by chronic treatment with astaxanthin. The 8-OHdG immunoreactive cells in glomeruli of non-treated db/db mice were more numerous than in the astaxanthin-treated db/db mice. In this study, treatment with astaxanthin ameliorated the progression and acceleration of diabetic nephropathy in the rodent model of type 2 diabetes. The results suggested that the antioxidative activity of astaxanthin reduced the oxidative stress on the kidneys and prevented renal cell damage. In conclusion, administration of astaxanthin might be a novel approach for the prevention of diabetes nephropathy.

Cancer prevention by carotenoids.
            (Nishino, 1998)  Download
Epidemiological investigations have shown that cancer risk is inversely related to the consumption of green and yellow vegetables and fruits. Since beta-carotene is present in abundance in these vegetables and fruits, it has been investigated extensively as a possible cancer-preventive agent. However, various carotenoids have also anti-carcinogenic activity. And we found that some of them, such as alpha-carotene, showed higher potency than beta-carotene to suppress carcinogenesis in animal experiments. Thus, we have carried out more extended studies on the cancer-preventive activities of natural carotenoids. For example, lutein, zeaxanthin, lycopene, phytoene, fucoxanthin, peridinin and astaxanthin seem to be promising. In the present study, we confirmed the anti-carcinogenic activities of fucoxanthin and peridinin. Among natural carotenoids, phytoene has not been evaluated precisely since it becomes unstable when it is purified. Here, the cancer-preventive activity of phytoene was demonstrated using new a biotechnological method; i.e., establishment of mammalian cells producing phytoene was followed by the introduction of crtB gene which encodes phytoene synthase, and these cells were proven to acquire the resistance against transformation imposed by transfection of activated oncogenes. Further studies on various natural carotenoids, besides beta-carotene, should be continued to get proper information regarding natural carotenoids in the field of cancer prevention.

Effects of astaxanthin on lipopolysaccharide-induced inflammation in vitro and in vivo.
            (Ohgami et al., 2003)  Download
PURPOSE:  Astaxanthin (AST) is a carotenoid that is found in marine animals and vegetables. Several previous studies have demonstrated that AST exhibits a wide variety of biological activities including antioxidant, antitumor, and anti-Helicobacter pylori effects. In this study, attention was focused on the antioxidant effect of AST. The object of the present study was to investigate the efficacy of AST in endotoxin-induced uveitis (EIU) in rats. In addition, the effect of AST on endotoxin-induced nitric oxide (NO), prostaglandin E2 (PGE2), and tumor necrosis factor (TNF)-alpha production in a mouse macrophage cell line (RAW 264.7) was studied in vitro. METHODS:  EIU was induced in male Lewis rats by a footpad injection of lipopolysaccharide (LPS). AST or prednisolone was administered intravenously at 30 minutes before, at the same time as, or at 30 minutes after LPS treatment. The number of infiltrating cells and protein concentration in the aqueous humor collected at 24 hours after LPS treatment was determined. RAW 264.7 cells were pretreated with various concentrations of AST for 24 hours and subsequently stimulated with 10 microg/mL of LPS for 24 hours. The levels of PGE2, TNF-alpha, and NO production were determined in vivo and in vitro. RESULTS:  AST suppressed the development of EIU in a dose-dependent fashion. The anti-inflammatory effect of 100 mg/kg AST was as strong as that of 10 mg/kg prednisolone. AST also decreased production of NO, activity of inducible nitric oxide synthase (NOS), and production of PGE2 and TNF-alpha in RAW264.7 cells in vitro in a dose-dependent manner. CONCLUSIONS:  This study suggests that AST has a dose-dependent ocular anti-inflammatory effect, by the suppression of NO, PGE2, and TNF-alpha production, through directly blocking NOS enzyme activity.

Growth-inhibitory effects of the astaxanthin-rich alga Haematococcus pluvialis in human colon cancer cells.
            (Palozza et al., 2009)  Download
The growth-inhibitory effects of the astaxanthin-rich Haematococcus pluvialis were studied in HCT-116 colon cancer cells. H. pluvialis extract (5-25 microg/ml) inhibited cell growth in a dose- and time-dependent manner, by arresting cell cycle progression and by promoting apoptosis. At 25 microg/ml of H. pluvialis extract, an increase of p53, p21(WAF-1/CIP-1) and p27 expression (220%, 160%, 250%, respectively) was observed, concomitantly with a decrease of cyclin D1 expression (58%) and AKT phosphorylation (21%). Moreover, the extract, at the same concentration, strongly up-regulated apoptosis by modifying the ratio of Bax/Bcl-2 and Bcl-XL, and increased the phosphorylation of p38, JNK, and ERK1/2 by 160%, 242%, 280%, respectively. Growth-inhibitory effects by H. pluvialis were also observed in HT-29, LS-174, WiDr, SW-480 cells. This study suggests that H. pluvialis may protect from colon cancer.

Astaxanthin supplementation does not augment fat use or improve endurance performance.
            (Res et al., 2013)  Download
INTRODUCTION:  Astaxanthin is a lipid-soluble carotenoid found in a variety of aquatic organisms. Prolonged astaxanthin supplementation has been reported to increase fat oxidative capacity and improve running time to exhaustion in mice. These data suggest that astaxanthin may be applied as a potent ergogenic aid in humans. PURPOSE:  To assess the effect of 4 wk of astaxanthin supplementation on substrate use and subsequent time trial performance in well-trained cyclists. METHODS:  Using a double-blind parallel design, 32 young, well-trained male cyclists or triathletes (age = 25 ± 1 yr, weight = 73 ± 1 kg, V˙O2peak = 60 ± 1 mL·kg·min, Wmax = 395 ± 7 W; mean ± SEM) were supplemented for 4 wk with 20 mg of astaxanthin per day (ASTA) or a placebo (PLA). Before and after the supplementation period, subjects performed 60 min of exercise (50% Wmax), followed by an time trial of approximately 1 h. RESULTS:  Daily astaxanthin supplementation significantly increased basal plasma astaxanthin concentrations from nondetectable values to 187 ± 19 μg·kg (P < 0.05). This elevation was not reflected in greater total plasma antioxidant capacity (P = 0.90) or attenuated malondialdehyde levels (P = 0.63). Whole-body fat oxidation rates during submaximal exercise did not differ between groups and did not change over time (from 0.71 ± 0.04 to 0.68 ± 0.03 g·min and from 0.66 ± 0.04 to 0.61 ± 0.05 g·min in the PLA and ASTA groups, respectively; P = 0.73). No improvements in time trial performance were observed in either group (from 236 ± 9 to 239 ± 7 and from 238 ± 6 to 244 ± 6 W in the PLA and ASTA groups, respectively; P = 0.63). CONCLUSION:  Prolonged astaxanthin supplementation does not augment antioxidant capacity, increase fat oxidative capacity, or improve time trial performance in trained cyclists.

Astaxanthin induces mitochondria-mediated apoptosis in rat hepatocellular carcinoma CBRH-7919 cells.
            (Song et al., 2011)  Download
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.

Effect of daily use of natural astaxanthin on C-reactive protein
            (Spiller et al., 2006a)  Download
Previous studies have provided data suggesting that daily use of natural astaxanthin can positively address inflammatory conditions such as rheumatoid arthritis and carpal tunnel syndrome. In this study, the effect of daily use of BioAstin™, a microalgae extract containing natural astaxanthin, on C-reactive protein was evaluated. It was found that after daily use of BioAstin for eight weeks C-reactive protein (CRP) was significantly lowered in the treatment group as compared to the placebo group. This correlation of reduced

Effect of daily use of natural astaxanthinon on symptoms associated with Tennis Elbow
            (Spiller et al., 2006b)  Download
Previous studies have provided data suggesting that daily use of natural astaxanthin can positively address inflammatory conditions such as rheumatoid arthritis and carpal tunnel syndrome. In this study, the effect of daily use of BioAstin™, a microalgae extract containing natural astaxanthin, on C-reactive protein was evaluated. It was found that after daily use of BioAstin for eight weeks C-reactive protein (CRP) was significantly lowered in the treatment group as compared to the placebo group. This correlation of reduced

Astaxanthin protects beta-cells against glucose toxicity in diabetic db/db mice.
            (Uchiyama et al., 2002)  Download
Oxidative stress induced by hyperglycemia possibly causes the dysfunction of pancreatic beta-cells and various forms of tissue damage in patients with diabetes mellitus. Astaxanthin, a carotenoid of marine microalgae, is reported as a strong anti-oxidant inhibiting lipid peroxidation and scavenging reactive oxygen species. The aim of the present study was to examine whether astaxanthin can elicit beneficial effects on the progressive destruction of pancreatic beta-cells in db/db mice--a well-known obese model of type 2 diabetes. We used diabetic C57BL/KsJ-db/db mice and db/m for the control. Astaxanthin treatment was started at 6 weeks of age and its effects were evaluated at 10, 14, and 18 weeks of age by non-fasting blood glucose levels, intraperitoneal glucose tolerance test including insulin secretion, and beta-cell histology. The non-fasting blood glucose level in db/db mice was significantly higher than that of db/m mice, and the higher level of blood glucose in db/db mice was significantly decreased after treatment with astaxanthin. The ability of islet cells to secrete insulin, as determined by the intraperitoneal glucose tolerance test, was preserved in the astaxanthin-treated group. Histology of the pancreas revealed no significant differences in the beta-cell mass between astaxanthin-treated and -untreated db/db mice. In conclusion, these results indicate that astaxanthin can exert beneficial effects in diabetes, with preservation of beta-cell function. This finding suggests that anti-oxidants may be potentially useful for reducing glucose toxicity.

Evaluation of the protective effects of all-trans-astaxanthin on canine osteosarcoma cell lines.
            (Wakshlag et al., 2010)  Download
OBJECTIVE:  To determine the effects of the antioxidant astaxanthin on growth of canine osteosarcoma cells with and without concurrent chemotherapeutic or irradiation insult. SAMPLE POPULATION:  Cells from 3 established canine osteosarcoma cell lines (D17, OS 2.4, and HMPOS). PROCEDURES:  Growth-curve kinetics and cell cytotoxic effects were assessed by means of various treatment combinations and a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Western blotting was performed to examine previously identified signaling pathways that astaxanthin reportedly affects. Additionally, cell-cycle kinetic evaluations, soft agar colony-forming assays, and antioxidant assays were performed to better understand the effect of astaxanthin on cell growth and function. RESULTS:  Exposure to astaxanthin alone resulted in a mild to pronounced attenuation of cell proliferation in vitro, depending on the cell line, and did not interfere with the cell-death response to doxorubicin, irradiation, or peroxide-mediated insult. In some instances, astaxanthin acted in an additive fashion to augment cell death. Astaxanthin exposure increased the antioxidant potential of cells, whereas peroxide-mediated cell stress increased the antioxidant potential to the same degree as astaxanthin exposure or greater. No dramatic changes in phosphorylation of protein kinase B or upregulation of connexin 43 were detected. CONCLUSIONS AND CLINICAL RELEVANCE:  Findings suggested that astaxanthin administration may be beneficial in treatment of dogs for osteosarcoma. Its actions as an antioxidant did not improve osteosarcoma cell survival during chemotherapeutic or irradiation insults, warranting further research into this natural compound as an adjuvant, antiproliferative treatment for osteosarcoma in dogs.


 

Astaxanthin upregulates heme oxygenase-1 expression through ERK1/2 pathway and its protective effect against beta-amyloid-induced cytotoxicity in SH-SY5Y cells.
            (Wang et al., 2010)  Download
Astaxanthin (ATX), the most abundant flavonoids in propolis, has been proven to exert neuroprotective property against glutamate-induced neurotoxicity and ischemia-reperfusion-induced apoptosis. Previous study have revealed that ATX can rescue PC12 cells from Aβ(25-35)-induced apoptotic death. However, the mechanisms by which ATX mediates its therapeutic effects in vitro are unclear. In the present study, we explored the underlying mechanisms involved in the protective effects of ATX on the Aβ(25-35)-induced cytotoxicity in SH-SY5Y cells. Pre-treatment with ATX for 4h significantly reduced the Aβ(25-35)-induced viability loss, apoptotic rate and attenuated Aβ-mediated ROS production. In addition, ATX inhibited Aβ(25-35)-induced lowered membrane potential, decreased Bcl-2/Bax ratio. We also demonstrated that ATX could prevent the activation of p38MAPK kinase pathways induced by Aβ. Moreover, we for the first time have revealed the ATX increased antioxidant enzyme heme oxygenase-1 (HO-1) expression in concentration-dependent and time-dependent manners, which were correlated with its protective effect against Aβ(25-35)-induced injury. Because the inhibitor of HO-1 activity, ZnPP reversed the protective effect of ATX against Aβ(25-35)-induced cell death. We also demonstrated that the specific ERK inhibitor, PD98059, concentration-dependently blocked on ATX-induced HO-1 expression, and meanwhile PD98059 reversed the protective effect of ATX against Aβ25-35-induced cell death. Taken together, these findings suggest that astaxanthin can induce HO-1 expression through activation of ERK signal pathways, thereby protecting the SH-SY5Y cells from Aβ(25-35)-induced oxidative cell death.

Dietary astaxanthin inhibits colitis and colitis-associated colon carcinogenesis in mice via modulation of the inflammatory cytokines.
            (Yasui et al., 2011)  Download
Astaxanthin (AX) is one of the marine carotenoid pigments, which possess powerful biological antioxidant, anti-inflammatory and anti-cancer properties. The purpose of this study is to investigate possible inhibitory effect of AX against inflammation-related mouse colon carcinogenesis and dextran sulfate sodium (DSS)-induced colitis in male ICR mice. We conducted two different experiments. In the first experiment, we evaluated the effects of AX at three dose levels, 50, 100 and 200 ppm in diet, on colitis-associated colon carcinogenesis induced by azoxymethane (AOM)/DSS in mice. In the second, the effects of the AX (100 and 200 ppm) in diet on DSS-induced colitis were determined. We found that dietary AX significantly inhibited the occurrence of colonic mucosal ulcers, dysplastic crypts, and colonic adenocarcinoma at week 20. AX-feeding suppressed expression of inflammatory cytokines, including nuclear factor (NF)-κB, tumor necrosis factor (TNF)-α and interleukin (IL)-1β, inhibited proliferation, and induced apoptosis in the colonic adenocarcinomas. Feeding with 200 ppm AX, but not 100 ppm, significantly inhibited the development of DSS-induced colitis. AX feeding (200 ppm in diet) also lowered the protein expression of NF-κB, and the mRNA expression of inflammatory cytokines, including IL-1β, IL-6, and cyclooxygenase (COX)-2. Our results suggest that the dietary AX suppresses the colitis and colitis-related colon carcinogenesis in mice, partly through inhibition of the expression of inflammatory cytokine and proliferation. Our findings suggest that AX is one of the candidates for prevention of colitis and inflammation-associated colon carcinogenesis in humans.

Supplemental cellular protection by a carotenoid extends lifespan via Ins/IGF-1 signaling in Caenorhabditis elegans.
            (Yazaki et al., 2011)  Download
Astaxanthin (AX), which is produced by some marine animals, is a type of carotenoid that has antioxidative properties. In this study, we initially examined the effects of AX on the aging of a model organism C. elegans that has the conserved intracellular pathways related to mammalian longevity. The continuous treatments with AX (0.1 to 1 mM) from both the prereproductive and young adult stages extended the mean lifespans by about 16-30% in the wild-type and long-lived mutant age-1 of C. elegans. In contrast, the AX-dependent lifespan extension was not observed even in a daf-16 null mutant. Especially, the expression of genes encoding superoxide dismutases and catalases increased in two weeks after hatching, and the DAF-16 protein was translocated to the nucleus in the AX-exposed wild type. These results suggest that AX protects the cell organelle mitochondria and nucleus of the nematode, resulting in a lifespan extension via an Ins/IGF-1 signaling pathway during normal aging, at least in part.

 


References

Liu, SZ, et al. (2018), ‘Building strength, endurance, and mobility using an astaxanthin formulation with functional training in elderly.’, J Cachexia Sarcopenia Muscle, 9 (5), 826-33. PubMed: 30259703
Malmsten, CL and A Lignell (2008), ‘Dietary Supplementation with Astaxanthin-Rich Algal Meal Improves Strength Endurance–A Double Blind Placebo Controlled Study on Male Students’, Carotenoid Sci, 13 20. PubMed:
Manabe, E, et al. (2008), ‘Astaxanthin protects mesangial cells from hyperglycemia-induced oxidative signaling.’, J Cell Biochem, 103 (6), 1925-37. PubMed: 17955498
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Nagendraprabhu, P and G Sudhandiran (2011), ‘Astaxanthin inhibits tumor invasion by decreasing extracellular matrix production and induces apoptosis in experimental rat colon carcinogenesis by modulating the expressions of ERK-2, NFkB and COX-2.’, Invest New Drugs, 29 (2), 207-24. PubMed: 19876598
Naito, Y, et al. (2004), ‘Prevention of diabetic nephropathy by treatment with astaxanthin in diabetic db/db mice.’, Biofactors, 20 (1), 49-59. PubMed: 15096660
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——— (2006b), ‘Effect of daily use of natural astaxanthinon on symptoms associated with Tennis Elbow’, On file at Cyanotech, PubMed:
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Wakshlag, JJ, et al. (2010), ‘Evaluation of the protective effects of all-trans-astaxanthin on canine osteosarcoma cell lines.’, Am J Vet Res, 71 (1), 89-96. PubMed: 20043787
Wang, HQ, et al. (2010), ‘Astaxanthin upregulates heme oxygenase-1 expression through ERK1/2 pathway and its protective effect against beta-amyloid-induced cytotoxicity in SH-SY5Y cells.’, Brain Res, 1360 159-67. PubMed: 20828541
Yasui, Y, et al. (2011), ‘Dietary astaxanthin inhibits colitis and colitis-associated colon carcinogenesis in mice via modulation of the inflammatory cytokines.’, Chem Biol Interact, 193 (1), 79-87. PubMed: 21621527
Yazaki, K, et al. (2011), ‘Supplemental cellular protection by a carotenoid extends lifespan via Ins/IGF-1 signaling in Caenorhabditis elegans.’, Oxid Med Cell Longev, 2011 596240. PubMed: 22013497