Astaxanthin and DNA protection -
Therefore, protecting the skin from UVB can prevent skin aging. The cells were incubated for 24 h after UVB exposure and cell viability was determined by MTT assay. Further, UVB increased the levels of DNA lesions such as cyclobutane pyrimidine dimer CPD and 8-hydroxyguanine 8-OHdG.
Conversely, RA decreased both CPD and 8-OHdG levels in a concentration-dependent manner. UVB exposure also increased phosphorylation of ataxia-telangiectasia mutated ATM protein kinase and p53 and subsequently increased the levels of GADD45 alpha, p21, and matrix metalloproteinases MMPs -3, -9, and Additionally, UVB exposure decreased the level of COL1A1.
However, RA treatment decreased the levels of p-ATM, p-p53, GADD45 alpha, p21, MMP-3, -9, and and increased the level of COL1A1 in a concentration-dependent manner. These results suggest that RA reduces UVB-induced cytotoxicity and genotoxicity through up-regulation of DNA repair via the combined effects of Rg2 and astaxanthin.
Subject Ultraviolet B Ginsenoside Rg2 Astaxanthin HaCaT cells. Additional Information Journal Title Animal Cells and Systems Rights Creative Commons Attribution-NonCommercial 4. Metadata Show full item record. Except where otherwise noted, this item's license is described as Creative Commons Attribution-NonCommercial 4.
Search ScholarWorks This Collection. Data Management FAQ Accessibility Contact Us. View Usage Statistics View Google Analytics Statistics.
Citation Tripathi, D N. Tripathi DN, Jena GB. Tripathi, D. Chemico-biological Interactions , 3 , Intervention of Astaxanthin Against Cyclophosphamide-induced Oxidative Stress and DNA Damage: a Study in Mice.
PubMed PMID: TY - JOUR T1 - Intervention of astaxanthin against cyclophosphamide-induced oxidative stress and DNA damage: a study in mice. Prime PubMed is provided free to individuals by: Unbound Medicine.
Related Citations Ebselen attenuates cyclophosphamide-induced oxidative stress and DNA damage in mice. Protective effects of total saponins from stem and leaf of Panax ginseng against cyclophosphamide-induced genotoxicity and apoptosis in mouse bone marrow cells and peripheral lymphocyte cells.
Oral administration of Cr VI induced oxidative stress, DNA damage and apoptotic cell death in mice. An evaluation, using the comet assay and the micronucleus test, of the antigenotoxic effects of chlorophyll b in mice. Induction of oxidative stress and DNA damage in cervix in acute treatment with benzo[a]pyrene.
Metformin does not prevent DNA damage in lymphocytes despite its antioxidant properties against cumene hydroperoxide-induced oxidative stress. Ellagic acid, a natural polyphenol protects rat peripheral blood lymphocytes against nicotine-induced cellular and DNA damage in vitro: with the comparison of N-acetylcysteine.
Protective effect of liposomal formulation of tuftsin a naturally occurring tetrapeptide against cyclophosphamide-induced genotoxicity and oxidative stress in mice. Astaxanthin inhibits cytotoxic and genotoxic effects of cyclophosphamide in mice germ cells.
Effective date Multivitamin for energy-boosting ;rotection Free format Astaxanthiin : ABANDONED -- FAILURE TO RESPOND TO Energy-boosting supplements for athletes Astaxanthin and DNA protection ACTION. Provided herein are methods for reducing oxidative DNA protecction in a subject, by administering to the DA astaxanthin, for instance a natural, astaxanthin-enriched extract from Haematococcus pluvialis. Provisional Patent Application No. This disclosure is related to reducing oxidative damage to DNA in cells, particularly in immune cells in mammals. More specifically, this disclosure provides methods of using a natural extract comprising and enriched in astaxanthin to reduce, prevent, or treat oxidative damage to DNA in mammals. The molecular reduction of oxygen to water during oxidative phosphorylation results inevitably in the production of superoxide radicals.Astaxanthin and DNA protection -
If you are located in the Netherlands you can purchase only at lifeextensioneurope. STAY AT LIFE EXTENSION EUROPE. Due to legal restrictions, we cannot provide you with detailed information about the products on the Dutch website.
If you would like to learn more about the products, you can do so in any language at lifeextensioneurope. To be able to use the full range of Shopware 6, we recommend activating Javascript in your browser. Antioxidants Back Take the quiz Customer care.
Anti-aging Memory Beauty non-GMO Skin Care Gluten-free Eyes Brain Astaxanthin Heart. Astaxanthin for immune, brain, vascular and eye health support. Item 4 mg 30 Softgels 1 per serving In Stock. For you, if you are interested in a powerful antioxidant that can support overall body health The ingredients in Astaxanthin with Phospholipids can: Support immune, brain, cardiovascular, mitochondrial health Cross the blood-eye barrier and support eye health Provide higher than normal absorbability Use Astaxanthin with Phospholipids to get most of the health benefits that astaxanthin can give you, from joint support to immune, brain, cardiovascular, mitochondrial and eye health support — astaxanthin can support it all!
Buy 1. Buy 2. Buy 4. Add to shopping cart. Money Back Guarantee We have a days return policy, not the standard 30 days! Daily Shipping Order before CET, for same day shipping Mon-Fri. Customer Care Advisory We can help you in 6 languages. Product details Supplement Facts Reference Product details "Astaxanthin with Phospholipids".
Health benefits at a glance: Astaxanthin is a very versatile antioxidant loaded with health benefits. Why it works: Astaxanthin is powerful antioxidant which can support over all body health and is a very important nutrient for eye health support.
The science behind the product: Astaxanthin is a red pigment molecule that is a member of the carotenoid family found in certain marine algae]. How to use: Take one 1 softgel once or twice daily with or without food, or as recommended by a healthcare practitioner. Health topics: Type Antioxidants.
Supplement Facts. Keep out of reach of children. Do not exceed recommended dose. Do not purchase if outer seal is broken or damaged. Biochimica et Biophysica Acta.
Chem Biol Interact. Eur J Nutr. Nutr Metab Lond. BMC Neurosci. FASEB J. J Clin Biochem Nutr. Brain Res. Forum Nutr. Biol Pharm Bull. Nutr Res. J Nutr. Cardiovasc Hematol Agents Med Chem.
Future Cardiol. Astaxanthin has been shown to reduce bacterial load and gastric inflammation in Helicobacter pylori -infected mice [ 5 ], and to protect against UVA-induced oxidative stress [ 8 ].
Immune cells are particularly sensitive to oxidative stress due to a high percentage of polyunsaturated fatty acids in their plasma membranes, and they generally produce more oxidative products [ 1 ]. Overproduction of reactive oxygen and nitrogen species can tip the oxidant:antioxidant balance, resulting in the destruction of cell membranes, proteins and DNA.
Therefore, under conditions of increased oxidative stress e. during disease states , dietary antioxidants become critical in maintaining a desirable oxidant:antioxidant balance. While studies on the immunomodulatory role of dietary astaxanthin have been reported in rodents, similar studies in humans are not available.
We hypothesize that dietary astaxanthin will act as a potent antioxidative and anti-inflammatory agent; through these and other mechanisms, astaxanthin can enhance immune response.
Our objective is to study the possible immune-enhancing, antioxidative and anti-inflammatory activity of dietary astaxanthin in humans. Free-living healthy female college students with an average age of Participants were recruited from Inha University Seoul, Korea through flyers and emails, and all were native Koreans.
Subjects with a history of diabetes, alcohol abuse, cancer or smoking were excluded; exclusion criteria also included those taking antioxidant supplements.
Prior to the initiation of dietary supplementation, a three-day dietary record was obtained from each subject who provided informed consent. During the study, subjects were allowed to consume their normal diets but were advised to refrain from eating astaxanthin-rich foods such as salmon, lobster, and shrimp.
Astaxanthin was administered as a softgel capsule taken every morning, and all softgel capsules were externally identical. Blinding was further ensured by assigning consecutive numbers to the dietary treatments and maintaining a master list until the study was completed.
The astaxanthin complex used in this study came from a supercritical CO 2 extract of Haematococcus pluvialis. Astaxanthin in the H. pluvialis extract is entirelythe 3S, 3S' enantiomer, and is primarily monoesterified with smaller quantities of diester and free astaxanthin.
To minimize subject-to-subject and assay-to-assay variation due to different sampling days, blood was drawn from all 42 subjects on one day for each of wk 0, 4 and 8.
Immune function and oxidative status was assessed within 24 h of blood collection. All procedures were approved by the Institutional Review Board IRB of Washington State University. Astaxanthin content in plasma was analyzed by reverse phase HPLC Alliance , Waters, Milford, MA as previously described [ 9 ].
Trans-β-apo-8'carotenal Sigma Chem. Louis, MO was used as the internal standard. Absorbance was monitored at nm on a photo diode array detector. Results were calculated as stimulation index. Effector cells peripheral blood mononuclear cells and target K cells were cultured at effector:target ratios of and in DMEM Sigma, St.
Killing was assessed using MTT to measure cell viability. The percent of specific cytotoxicity was calculated as follows:. Cells were labeled with monoclonal antibodies conjugated to fluorescein isothiocyanate FITC or phycoerythrin PE : anti-CD3 was conjugated to FITC, and anti-CD8, anti-CD4 and anti-CD19 were conjugated to PE Caltag Laboratories, Burlingame, CA.
A lymphocyte analysis gate and the antibodies CDFITC and CDPE Caltag Laboratories, Burlingame, CA were used to help distinguish the lymphocytes from other blood cell types. A total of gated events were acquired for each sample and analyzed by flow cytometry FACScan, BD Biosciences, San Jose, CA using the Cell Quest program version 3.
Delayed-type hypersensitivity DTH response to an intracutaneous injection of tuberculin Mono-Vacc Test O. A physician administered the injections and also measured skin thickness and induration at 0, 24, 48 and 72 h after challenge. C-Reactive protein CRP , a well-established marker of inflammatory status, was measured in plasma with a commercially available ELISA Alpha Diagnostic, San Antonio, TX.
Oxidative DNA damage was assessed by measuring plasma 8-hydroxy-2'-deoxyguanosine 8-OHdG using competitive ELISA BIOXYTECH ® 8-OHdG-EIA Kit, OxisResearch, Portland, OR. Plasma concentrations of 8-epi-prostaglandin F2α 8-isoprostane were measured by a commercially available competitive ELISA 8-Isoprostane EIA kit, Cayman Chemical Company, Ann Arbor, MI.
Data were analyzed by repeated measures ANOVA using the General Linear Model of SAS [ 12 ]. Astaxanthin was not detectable in the plasma of any subjects at wk 0 or in the conrol group at wk 4 or 8.
However, concentrations of astaxanthin in plasma increased to maximal concentrations by wk 4 in a dose-dependent manner Figure 1. Dietary recall showed no treatment difference in daily dietary intake Table 1. Concentrations of plasma astaxanthin in human subjects fed 0, 2 or 8 mg astaxanthin daily for 8 wk.
Values are means; variation is expressed as a representative overall standard error. Both concentrations of each mitogen showed similar trends whether mitogens were low or high concentration. No differences in response were observed in 2Asta. Lymphocyte proliferation induced with phytohemagglutinin, concanavalin A and pokeweed mitogen in human subjects fed 0, 2 or 8 mg astaxanthin daily for 8 wk.
Values are means ± SEM. On the other hand, dietary astaxanthin did not significantly influence the population of Th, Tc or NK cells or the ratio of Th:Tc cells Table 2.
Supplemental astaxanthin did not have a significant effect on the expression of the cell surface adhesion molecules ICAM-1 CD54 and LFA-3 CD58 data not shown. DTH response was maximal at 48 to 72 h post-challenge Figure 3.
Delayed-type hypersensitivity tuberculin test in human subjects fed 0, 2 or 8 mg astaxanthin daily for 8 wk. Values are means ± overall standard error. No differences in TNF-α and IL-2 levels were seen in any treatments Table 3. However, higher dietary astaxanthin amounts did not influence the concentration of this acute phase protein.
Plasma concentrations of plasma C-reactive protein in human subjects fed 0, 2 or 8 mg astaxanthin daily for 8 wk. DNA damage observed with 2Asta was not further decreased in the group fed higher dietary astaxanthin 8Asta.
Concentrations of plasma 8-hydroxy-2'-deoxyguanosine in human subjects fed 0, 2 or 8 mg astaxanthin daily for 8 wk. Dietary astaxanthin did not significantly influence concentrations of plasma 8-isoprostane at all periods studied.
The overall mean concentration of 8-isoprostane was While the biological action of astaxanthin has been reported in both in vitro and in vivo studies, these have mainly used rodents and in vitro models.
This is the first comprehensive study to examine the action of dietary astaxanthin in regulating immune response, oxidative damage and inflammation in humans. Dietary astaxanthin enhanced both cell-mediated and humoral immune responses in young healthy feamles. The immune markers significantly enhanced by feeding astaxanthin included T cell and B cell mitogen-induced lymphocyte proliferation, NK cell cytotoxic activity, IFN-γ and IL-6 production, and LFA-1 expression.
Enhancement of these ex vivo immune markers corresponded with increased number of circulating total T and B cells. In addition, subjects given astaxanthin also showed an enhanced tuberculin DTH response, a reliable clinical test to assess in vivo T cell function. All of these immune responses were generally observed after 8 wk of supplementation following a cutaneous tuberculin injection.
Modulatory actions of astaxanthin on immune response have been demonstrated in both in vitro and in vivo studies. We previously reported higher mitogen-induced splenocyte proliferation in mice [ 4 ], dogs [ 13 ] and cats [ 14 ] fed astaxanthin.
Astaxanthin stimulated cell proliferation of murine splenocytes and thymocytes in vitro [ 15 ]. Others have shown that astaxanthin increased cytotoxic T lymphocyte activity in mice [ 16 ] and inhibited stress-induced suppression of NK cell activity [ 17 ].
In this study, astaxanthin heightened NK cell cytotoxic activity. Natural killer cells serve in an immuno-surveillance capacity against tumors and virus-infected cells; therefore, astaxanthin may play a role in cancer etiology.
Patients with Chediak-Higashi syndrome, a disorder associated with defective NK cell function, are indeed more susceptible to tumor formation.
Flow cytometry data showed higher subpopulations of total T and B cells. Activated T cells and NK cells produce IFN-γ, which is involved in immune-regulation, B cell differentiation, and antiviral activity.
IFN-γ production was higher in subjects supplemented with astaxanthin, similar to the response in mice given astaxanthin [ 16 ]. Splenocytes of tumor-bearing mice fed lutein also had higher IFN-γ expression, and these changes paralleled the inhibitory action of lutein against tumor growth [ 18 ].
Modulation of the humoral immune response also occurs; astaxanthin increased antibody production in mouse splenocytes [ 19 ], partially restored humoral immune response in old mice [ 6 ], enhanced immunoglobulin production in response to T-dependent stimuli in human blood cells [ 20 ] and induced production of polyclonal antibodies G and M in murine spleen cells [ 15 ].
The present study suggests that the higher antibody production may be due to an increase in B cell number. The skin tuberculin test is a reliable clinical test to assess in vivo T cell function. This study shows that subjects given astaxanthin had a heightened DTH response, which is also seen in dogs [ 13 ] and cats fed astaxanthin [ 14 ], β-carotene [ 10 , 14 ] and lutein [ 21 , 22 ].
Leukocyte function antigens LFA mediate intercellular adhesion between leukocytes and other cells in an antigen non-specific fashion. LFA-1 is a β 2 -integrin expressed on leukocytes involved in the migration of lymphocytes, monocytes and neutrophils. LFA-1 binds to ICAM-1 and ICAM-2 expressed on vascular endothelium, and controls lymphocyte migration into inflammatory sites.
Endothelial expression of ICAM-1 is inducible while ICAM-2 is constitutive. Therefore, the heightened DTH response in this study is likely due to an increased expression of LFA-1 but not ICAM.
Dietary astaxanthin dramatically decreased one DNA damage biomarker plasma 8-OHdG , and this protective effect was observed by wk 4 of feeding. Maximal response was observed with the lower 2 mg astaxanthin dose. In addition, subjects fed 2 mg astaxanthin also showed lower plasma C-reactive protein concentrations, demonstrating the anti-inflammatory action of astaxanthin in humans.
Immune cells are particularly sensitive to membrane damage by free radicals. Reactive oxygen species ROS are produced via the mitochondria electron transport system during ATP production, xanthine oxidase and phagocytes [ 23 , 24 ].
In fact, cumulative oxidative damage to the mitochondria is considered the main culprit of cell senescence which in turn is responsible for aging and the development of age-related chronic diseases [ 25 ].
The ROS can induce redox-sensitive transcription factors such as NFkB and AP-1, which regulate genes controlling production of chemokines, inflammatory cytokines, and adhesion molecules which stimulate phagocytic infiltration [ 26 ].
Conversely, astaxanthin, acting as a potent antioxidant, can inhibit ROS-induced production of these transcription factors, thereby decreasing inflammation.
Indeed, astaxanthin attenuated exercise-induced neutrophil infiltration and subsequent delayed-onset damage to the gastronemius and heart muscle in mice [ 26 ]. Astaxanthin is reported to be approximately fold more protective than lutein and β-carotene against UVA-induced oxidative stress in vitro [ 8 ].
Reactive nitrogen species also play an important role in inflammation. As with ROS, astaxanthin has been reported to decrease the production of nitric oxide NO and iNOS activity in a mouse macrophage cell line, resulting in the inhibition of COX which down-regulates the production of PGE 2 and TNF-α [ 27 ].
TNF-α is a pleiotropic cytokine produced by activated macrophages and monocytes, and has nonspecific resistance against various infectious agents.
Similarly, Lee et al. The TNF-α and IL-1 cascade activates p38 MAPK, thus promoting proinflammatory gene expression and cytokine production. Therefore, in this study, astaxanthin exerted its anti-inflammatory action by inhibiting reactive oxygen and nitrogen species. Why dietary astaxanthin did not reduce lipid peroxidation is unclear.
Astaxanthin has been shown to be one of the most effective antioxidants against lipid peroxidation and oxidative stress in in vitro and in vivo systems [ 3 , 29 ].
Humans given 1. The potent antioxidant activity of astaxanthin is likely due to the presence of a keto- and a hydroxyl group on each end of its molecule. This structural property effectively rigidifies cell membranes, thereby limiting the penetration of lipoperoxidation promoters across the lipid bilayer [ 32 ].
The isoprostane methodology used in this study lacks sensitivity and accuracy; this may account for the lack of a significant effect seen in this study. Taken together, the immunomodulatory, antioxidative and anti-inflammatory activity of astaxanthin will likely influence the etiology of cancer and inflammatory diseases.
Astaxanthin was more active than β-carotene, lutein and canthaxanthin in inhibiting mammary tumor growth in mice [ 7 ]. Others have reported that astaxanthin protected against carcinogenesis of the urinary bladder [ 33 ], decreased cancerous growth of the mouth [ 34 ], and decreased the number and size of liver preneoplastic foci [ 35 ] in rodents.
Astaxanthin, as an algal extract, protected UVA-induced DNA damage in human skin fibroblasts IBR-3 , melanocytes HEMAc and intestinal CaCo2 cells [ 36 ]. In addition, astaxanthin ameliorated other oxidative stress-induced inflammatory diseases such as diabetic nephropathy in diabetic mice [ 37 ], lipopolysaccharide-induced uveitis in rats [ 27 ], and exercise-induced skeletal and cardiac muscle damage in mice [ 26 ].
The polar ends if the astaxanthin structure allows it span biological membranes; this transmembrane alignment allows astaxanthin to preserve the membrane structure [ 38 ], decrease membrane fluidity [ 39 ], and function as an antioxidant [ 40 ].
These and other mechanisms may explain the antioxidative, anti-inflammatory and immune-modulatory action of astaxanthin. In this study, plasma concentrations of astaxanthin in subjects given 2 or 8 mg astaxanthin daily for 4 wk increased to 0. These plasma concentrations are lower than that reported by Osterlie et al.
The difference in plasma concentrations in the two human studies is expected, due to differences in the dose and length of astaxanthin administration; however, the two studies also used different sources of astaxanthin and different subject gender and age.
Most of the astaxanthin was found in the VLDL chylomicra, with lesser amounts in the LDL and HDL [ 41 ]. While the stereoisomer form of astaxanthin was not identified in this study, Osterlie et al. Astaxanthin used in the present study is from Haematococcus pluvialis and exists primarily in an esterified 3S, 3'S stereoisomer while synthetic astaxanthin [ 41 ] is primarily the 3R, 3'S form.
The amount of supplemental astaxanthin used in this study is achievable through diet means. Wild salmon contains the 3S, 3S' form of astaxanthin almost exclusively. The 3R, 3R' form is found rarely in nature but does exist in some crustaceans such as in Krill.
In healthy humans, 6 mg astaxanthin from H. pluvialis algal extract can be safely consumed [ 44 ]. Overall, this study shows that dietary astaxanthin enhanced immune response, and decreased a DNA oxidative damage biomarker and inflammation in young healthy females.
It is the initial scope of the study to focus on a narrow population with regards to age, gender and race; however, antioxidants generally show greater physiologic modulation under excess amounts of oxidative stress, in immuno-compromised individuals, and with longer feeding periods.
These likely explain the lack of efficacy in certain response measures studied. Future studies with astaxanthin administration will include these parameters. However, our present study suggests astaxanthin to be a bioactive natural carotenoid that may be important to human health.
Chew BP, Park JS: Carotenoids Against Disease: Part C: The Immune System and Disease. Carotenoids: Nutrition and Health.
Edited by: Britton G, Liaanen-Jensen S, Pfander H. Chapter Google Scholar. J Nutr. CAS Google Scholar. Kurashige M, Okimasu E, Inoue M, Utsumi K: Inhibition of oxidative injury of biological membranes by astaxanthin.
Physiol Chem Phys Med NMR. Chew BP, Wong MW, Park JS, Wong TS: Dietary β-carotene and astaxanthin but not canthaxanthin stimulate splenocyte function in mice. Anticancer Re. Bennedsen M, Wang X, Willen R, Wadstrom T, Andersen LP: Treatment of H. pylori infected mice with antioxidant astaxanthin reduces gastric inflammation, bacterial load and modulates cytokine release by splenocytes.
Immunol Lett. Article CAS Google Scholar. Jyonouchi H, Zhang L, Gross M, Tomita Y: Immunomodulating actions of carotenoids: enhancement of in vivo and in vitro antibody production to T-dependent antigens. Nutr Cancer. Chew BP, Park JS, Wong MW, Wong TS: A comparison of the anticancer activities of dietary β-carotene, canthaxanthin and astaxanthin in mice in vivo.
Anticancer Res. O'Connor I, O'Brien NM: Modulation of UVA light-induced oxidative stress by β-carotene, lutein and astaxanthin in cultured fibroblasts. J Dermatol Sci. Article Google Scholar. Chew BP, Park JS, Wong TS, Kim HW, Weng BB, Byrne KM, Hayek MG, Reinhart GA: Dietary β-carotene stimulates cell-mediated and humoral immune response in dogs.
Ryan-Borchers TA, Park JS, Chew BP, McGuire MK, Fournier LR, Beerman KA: Soy isoflavones modulate immune function in healthy postmenopausal women. Am J Clin Nutr. Google Scholar. Chew BP, Park JS, Hayek MG, Massimino S, Reinhart GA: Cell-mediated and humoral immune response in dogs fed astaxanthin.
Astaxabthin Item Goji Berry Hair Health Det medisinske fakultet Institutt for anv basalfag Ernæringsvitenskap View Item. JavaScript is Multivitamin for energy-boosting for your browser. Some features of this site may not work without it. Astaxanthin : a putative modulator of DNA damage and repair Hjorth, Marit. Master thesis. substring 0, gaValue. Open Multivitamin for energy-boosting peer-reviewed chapter. Submitted: 18 February Reviewed: Astxxanthin June Published: 26 September Gut health and weight loss Edited by Pdotection Queiroz Astaxanthih, Eduardo Jacob-Lopes Astaxahthin Veridiana Vera De Rosso. com Astaxanthin and DNA protection cbspd. The chapter is devoted to study the effects of astaxanthin on the frequency of chromosomal aberrations and the level of DNA damages in human peripheral blood lymphocytes under ionizing radiation exposure in vitro. To achieve the purpose of the research, a combination of classical cytogenetic methods G0- and G2-radiation sensitivity assays and method of single-cell electrophoresis comet assay was used.
0 thoughts on “Astaxanthin and DNA protection”