Astaxanthin
Last edited 10/07/2019 07:45:20 PM by Anthony Russano (anthony@qualitywebsolutions.org)


Astaxanthin is a keto-carotenoid. It belongs to a larger class of chemical compounds known as terpenes built from five carbon precursors, isopentenyl diphosphate, and dimethylallyl diphosphate.

Healing Properties

Antioxidant

Astaxanthin is the most powerful natural carotenoid antioxidant.[1]

Antiinflammatory

Astaxanthin decreases oxidative stress and inflammatory response in cells.[1]

Anticancer

Astaxanthin works together with Human serum albumin (the most abundant protein in blood plasma) to fight cancer at a cellular level.[2]

Antiproliferative

Astaxanthin was shown to prevent cell proliferation, Migration, And drug-resistance in human ovarian carcinoma cells.[2]

  • Astaxanthin induced apoptosis in carcinoma cells via mitochondrial apoptotic pathways.[2]

Cardioprotective

Astaxanthin is beneficial for ischemic-reperfusion of clogged arteries to help restore blood flow.[1]

Immunomodulator (Immune Response)

Mental Wellness (mental health)

Astaxanthin supplementation improves global mood state and supports mental wellness in healthy subjects.[3]

Neuroprotection (neuroprotective)

Astaxanthin's antioxidant properties provide powerful neuroprotection.

  • Short-term (7-day) treatment with astaxanthin demonstrated a protective effect on glial and neuronal alterations.[4]
    • glia are the connective tissue of the nervous system, they are associated with neurons which are the nerve cells.

Renal Health

Astaxanthin can increase peritubular capillary density (peritubular capillaries are tiny blood vessels in the renal system).[5]

  • Astaxanthin upregulates vascular endothelial growth factor and downregulates thrombospondin levels.[5]

Skin Health

Vision (eyesight)

Patients treated with lutein/zeaxanthin and astaxanthin together with antioxidants nutrients were more likely to report clinically meaningful stabilization/improvements in Visual Acuity, Contrast Sensitivity, and visual function through 24 months compared with non-treated subjects.[6]

Disease / Symptom Treatment

Chemotherapy

Retinal Toxicity

Retinal toxicity refers to toxicity of the retina in the eyes.

The astaxanthin molecule is a promising option to prevent retinal toxicity in patients receiving the antineoplastic (anti-cancer) agent, Cisplatin as treatment for malignant tumors.[7]

  • Astaxanthin treatment reduced the increases in MDA, eNOS, and 8-OHdG levels following CIS administration and increased the levels of GSH expressions, as well.[7]

Depression

Natural astaxanthin supplementation reduces negative mood state (depression and fatigue) and improves global mood state and thus supports mental wellness in healthy subjects.[3]

  • Significant improvements were found with Natural astaxanthin treatment for positive mood state.[3]

Diabetes

Dyslipidemia

Vision Loss

The carotenoid Astaxanthin can confer a rapid antioxidant protective effect to the retina.[4]

  • A high-fat diet and obesity coupled with type 2 diabetes can cause a condition called non-proliferative diabetic retinopathy. This is the most common cause of vision loss among people with diabetes.

Short-term treatment with astaxanthin has been shown to prevent glial dysfunction in the diabetic retina.[4]

Astaxanthin's antioxidant and neuroprotective properties can help attenuate the Retinal Changes caused by diabetic retinopathy.[4]

  • Diabetic retinopathy affects blood vessels in the light-sensitive tissue that lines the back of the eye (the retina). The blood vessels swell and develop balloon-like micro-aneurysms that leak fluid into the retina.

Fatigue

Heart Disease

Heart Attack

Hypertension

Renal Interstitial Fibrosis

Anti-fibrotic: Astaxanthin has been shown to attenuate renal interstitial fibrosis and peritubular capillary rarefaction via inactivation of the TGF‑β1/Smad signaling pathway.[5]

Nicotine-induced Toxicity

Astaxanthin protects the organs against the toxic effects of nicotine.[1]

  • Nicotine can cause harmful effects on the male testes potentially impacting fertility. Astaxanthin demonstrated a protective effect on these organs.[1]
    • Astaxanthin reversed the negative effects of nicotine.[1]

Vision Loss

  • Astaxanthin can be used as a supplementary medication for dry type-age related macular degeneration patients.[7]

Sources:

  1. Study Type: Animal Study
    Title: Histopathological Analysis of Testis: Effects of Astaxanthin Treatment against Nicotine Toxicity
    Author(s): Bashir Sobhani, Sahar Roomiani, Zahra Ahmadi, Milad Ashrafizadeh
    Institution(s): Ferdowsi University of Mashhad: Mashhad, Razavi Khorasan; Tabriz University: Tabriz, East Azerbaijan;
    Publication: Arak University of Medical Sciences
    Date: Feb 2019
    Abstract: Background: Nicotine is a toxic compound in the cigarette smoke and has destructive effects on various human organs. Astaxanthin is a carotenoid with high antioxidant property. In this study, we investigated the protective effects of astaxanthin against nicotine-induced toxicity in mice testes. Methods: Forty-two inbred balb/c male mice were divided into six groups:Group 1, received 1 ml normal saline daily; Group 2, received nicotine (1.5mg/kg); Group 3, received astaxanthin (25mg/kg); Group 4, received astaxanthin (50mg/kg); Group 5, received astaxanthin (25mg/kg) plus nicotine (1.5mg/kg); and group 6, received astaxanthin (50mg/kg) plus nicotine (1.5mg/kg). After collecting testes samples, microscopic slides were prepared at the School of Veterinary Medicine, University of Mashhad, and the prepared slides were examined under light microscopy. Results: The histological structures of the testes were normal in the control group and those receiving astaxanthin, regardless of nicotine (groups 3, 4, 5 & 6). However, group 2 that received only nicotine, showed transformed testicular histology with severe hemorrhage. Conclusion: Based on the results, nicotine caused harmful effects on the mice testes and astaxanthin appeared to protect the organs against the toxic effects of nicotine.
    Link: Source
    Citations:

  2. Study Type: Human Study: In Vitro
    Title: Astaxanthin Combine With Human Serum Albumin To Abrogate Cell Proliferation, Migration, And Drug-Resistant In Human Ovarian Carcinoma SKOV3 Cells
    Author(s): Xiu-Zhen Su, Ran Chen, Cai-Bing Wang, Xi-Lin Ouyang, Yan Jiang, Ming-Yi Zhu.
    Institution(s): Youjiang Medical University for Nationalities, 98 Chengxiang Road, Baise 533000, China
    Publication: Anti-Cancer Agents in Medicinal Chemistry
    Date: Feb 2019
    Abstract: Background: Astaxanthin (AST) shows a large range of beneficial effects together with anti-cancer and antioxidation properties. Human serum albumin (HSA) is the most abundant protein in blood plasma which plays the role of depot and transport protein for many exogenous compounds. However, whether HSA could enhance AST-induced cytotoxic effects in human ovarian cancer cells has not been examined to date. Objective: This study aims to explore the anticancer effect and the molecular mechanism of AST combine with HSA induced cytotoxicity in ovarian cancer SKOV3 cells. Method: The ovarian cancer SKOV3 cells were treated by AST combined with HSA to study the effects of cell proliferation, cell morphology, cell cycle arrest, related protein expression, nuclear transfer, cell migration, and drug-resistant. Results: Our data confirmed that AST+HSA treatment enhanced the anticancer effects of AST, arrested G1 phase cell cycle and induced apoptosis in SKOV3 cells. AST+HSA induced apoptosis via mitochondrial apoptotic pathways was related to the increased ratio of Bcl-2/Bax and activation of caspase-3. Besides, exposure of cells to AST+HSA triggered the inactivation of NF-κB and activation p53 and MAPKs signaling pathways. Furthermore, AST+HSA significantly overcome the drug-resistant and inhibited the migration of SKOV3 cells. Conclusion: AST combined treatment with HSA considerably inhibited NF-κB expression and translocation to nucleus, thereby improving the AST-induced cytotoxic effect on SKOV3 cells. These findings may provide rationale to combine AST with HSA for the treatment of ovarian cancer
    Link: Source
    Citations:

  3. Study Type: Human Study
    Title: Astaxanthin Supplementation Reduces Depression and Fatigue in Healthy Subjects
    Author(s): Shawn Talbott, Don Hantla, Bob Capelli, Lixin Ding, Yanmei Li and Christian Artaria
    Institution(s): EQQIL, Draper, UT, USA Treehouse Athletic Club, Draper, UT, USA, Algae Health Sciences, Irvine, CA, USA North America, Irvine, California, USA, Beijing, China, Europe, Lugano, Switzerland
    Publication: EC Nutrition
    Date: January 2019
    Abstract: Natural Astaxanthin from Haematococcus pluvialis microalgae (NAX) has been researched in hundreds of clinical trials, pre-clinical animal studies and in-vitro surveys for various bioactive properties that indicate potential preventive and therapeutic health benefits. Among the most widely-researched properties of astaxanthin in the literature are broad-spectrum anti-inflammato-ry activity and powerful antioxidant capacity. In addition, both human and animal research have revealed a wide range of potential benefits for neurological and eye health, cardiovascular function, exercise endurance, enhancement of the immune response and skin health. This study’s goal was to explore the effects of a daily dose of 12 mg per day of NAX on psychological mood state in healthy subjects.
    Link: Source
    Citations:

  4. Study Type: Animal Study
    Title: Short-Term Administration of Astaxanthin Attenuates Retinal Changes in Diet-Induced Diabetic Psammomys obesus
    Author(s): Baccouche B, Benlarbi M, Barber AJ, Ben Chaouacha-Chekir R
    Institution(s): Laboratoire de Physiopthologies, Alimentations et Biomolécules (PAB), Institut Supérieur de Biotechnologie de Sidi Thabet (ISBST), Univ Manouba (UMA), BiotechPole Sidi Thabet, Ariana, Tunisie; Faculté des Sciences de Bizerte (FSB), Université de Carthage (UCAR), Tunis, Tunisie; Department of Ophthalmology; Penn State Hershey Eye Center, Milton S. Hershey Medical Center, Penn State College of Medicine, Hershey, PA, USA
    Publication: Current Eye Research
    Date: Sept 2018
    Abstract: OBJECTIVES: Psammomys obesus is a high-fat diet (HFD)-fed animal model of obesity and type 2 diabetes recently explored as a model of non-proliferative diabetic retinopathy. This study tested the protective effect of the pigment astaxanthin (AST) in the P. obesus diabetic retina. METHODS: Young adult P. obesus were randomly assigned to two groups. The control group received a normal diet consisting of a plant-based regimen, and the HFD group received an enriched laboratory chow. After 3 months, control and diabetic rodents were administered vehicle or AST, daily for 7 days. Body weight, blood glucose, and plasma pentosidine were assessed. Frozen sections of retinas were immunolabeled for markers of oxidative stress, glial reactivity and retinal ganglion cell bodies, and imaged by confocal microscopy. RESULTS: Retinal tissue from AST-treated control and HFD-diabetic P. obesus showed a greater expression of the antioxidant enzyme heme oxygenase-1 (HO-1). In retinas of HFD-diabetic AST-treated P. obesus, cellular retinaldehyde binding protein and glutamine synthetase in Müller cells were more intense compared to the untreated HFD-diabetic group. HFD-induced diabetes downregulated the expression of glial fibrillary acidic protein in astrocytes, the POU domain protein 3A in retinal ganglion cells, and synaptophysin throughout the plexiform layers. DISCUSSION: Our results show that type 2-like diabetes induced by HFD affected glial and neuronal retinal cell homeostasis. AST treatment induced the antioxidant enzyme HO-1 and reduced glial reactivity. These findings suggest that diabetic P. obesus is a useful model of HFD-induced obesity and diabetes to evaluate early neuroglial retinal alterations and antioxidant neuroprotection mechanisms in DR.
    Link: Source
    Citations:

  5. Study Type: Animal Study
    Title: Astaxanthin ameliorates renal interstitial fibrosis and peritubular capillary rarefaction in unilateral ureteral obstruction
    Author(s): Jin Zhao Meixia Meng Jinhua Zhang Lili Li Xiaojing Zhu Li Zhang Chang Wang Ming Gao
    Institution(s): Department of Nephrology, Xi'an No. 4 Hospital, Xi'an, Shaanxi 710004, P.R. China
    Publication: Spandidos Publications: Molecular Medicine Reports
    Date: February 2019
    Abstract: Loss of peritubular capillaries is a notable feature of progressive renal interstitial fibrosis. Astaxanthin (ASX) is a natural carotenoid with various biological activities. The present study aimed to evaluate the effect of ASX on unilateral ureteral obstruction (UUO)‑induced renal fibrosis in mice. For that purpose, mice were randomly divided into five treatment groups: Sham, ASX 100 mg/kg, UUO, UUO + ASX 50 mg/kg and UUO + ASX 100 mg/kg. ASX was administered to the mice for 7 or 14 days following UUO. The results demonstrated that UUO‑induced histopathological changes in the kidney tissue were prevented by ASX. Renal function was improved by ASX treatment, as evidenced by decreased blood urea nitrogen and serum creatinine levels. Furthermore, the extent of renal fibrosis and collagen deposition induced by UUO was suppressed by ASX. The levels of collagen I, fibronectin and α‑smooth muscle actin were increased by UUO in mice or by transforming growth factor (TGF)‑β1 treatment in NRK‑52E cells, and were reduced by ASX administration. In addition, ASX inhibited the UUO‑induced decrease in peritubular capillary density by upregulating vascular endothelial growth factor and downregulating thrombospondin 1 levels. Inactivation of the TGF‑β1/Smad signaling pathway was involved in the anti‑fibrotic mechanism of ASX in UUO mice and TGF‑β1‑treated NRK‑52E cells. In conclusion, ASX attenuated renal interstitial fibrosis and peritubular capillary rarefaction via inactivation of the TGF‑β1/Smad signaling pathway.
    Link: Source
    Citations:

  6. Study Type: Human Study: open-label randomized study
    Title: Carotenoids in Age-related Maculopathy Italian Study (CARMIS): two-year results of a randomized study.
    Author(s): Piermarocchi S1, Saviano S, Parisi V, Tedeschi M, Panozzo G, Scarpa G, Boschi G, Lo Giudice G; Carmis Study Group.
    Institution(s): Department of Ophthalmology, University of Padova, Padova, Italy.
    Publication: European Journal of Ophthalmology
    Date: March 2012
    Abstract: PURPOSE: The high concentration of carotenoids in the macula, plus evidence linking oxidative stress to age-related macular degeneration (AMD) and carotenoids to antioxidation, generated the hypothesis that higher antioxidant intakes can prevent AMD. The aim of this study was to determine whether nutritional supplementation with a targeted nutritional supplement improves visual acuity and visual function in AMD. METHODS: In this multicenter, prospective open-label randomized study, 145 patients were randomly assigned to 2 different treatment groups. Interventions were lutein (10 mg), zeaxanthin (1 mg), astaxanthin (4 mg; AZYR SIFI, Catania, Italy), and antioxidants/vitamins supplementation formula or no dietary supplementation for 2 years. Primary outcome was mean changes in visual acuity (VA) at 12 and 24 months. Other measures included contrast sensitivity (CS) and National Eye Institute visual function questionnaire (NEI VFQ-25) scores at 12 and 24 months. RESULTS: Patients in the treated group showed stabilization of VA with significantly (p=0.003) better VA scores (81.4 ± 7.2) compared to the nontreated group (76.8 ± 8.9) at 24-month follow-up. An improvement in CS (p=0.001) and final mean NEI VFQ-25 composite scores at 12 and 24 months higher in treated group compared to nontreated group were also shown (p<0.001). CONCLUSIONS: Patients treated with lutein/zeaxanthin and astaxanthin together with other nutrients were more likely to report clinically meaningful stabilization/improvements in VA, CS, and visual function through 24 months compared with nontreated subjects. Further studies are needed with more patients and for longer periods of time.
    Link: Source
    Citations:

  7. Study Type: Animal Study
    Title: The protective effects of astaxanthin against cisplatin-induced retinal toxicity
    Author(s): Hüseyin Fındık, Levent Tumkaya, Adnan Yılmaz, Mehmet Gökhan Aslan, Murat Okutucu, Kerimali Akyildiz & Tolga Mercantepe
    Institution(s): Department of Ophthalmology, Faculty of Medicine, Recep Tayyip Erdogan University, 53100, RizebDepartment of Histology and Embryology, Faculty of Medicine, Recep Tayyip Erdogan University, 53100, RizecDepartment of Biochemistry, Faculty of Medicine, Recep Tayyip Erdogan University, 53100,RizedDepartment of Medical Services and Techniques, Health Care Services Vocational School, Recep Tayyip Erdogan University, 53100, Rize
    Publication: Cutaneous and Ocular Toxicology
    Date: January 2019
    Abstract: Purpose: This study investigated the toxic effects of an antineoplastic agent, cisplatin (CIS), on retinal cells and the potential capacity of astaxanthin (ASTA) to elicit a future therapeutic protocol in CIS-induced retinal toxicity. Materials and methods: Six groups were formed for the assessment; control (healthy; Group 1), olive oil (olive oil only; Group 2), ASTA control group (ASTA only, Group 3), the single intraperitoneal (IP) dose of 16 mg/kg CIS (CIS only group; Group 4), 16 mg/kg CIS +25 mg/kg (IP) ASTA (Group 5), and 16 mg/kg CIS +75 mg/kg (IP) ASTA (Group 6). On the third day after CIS administration, rats in all groups were sacrificed under anesthesia and the analysis of the biochemical parameters and histopathological levels were performed. Results: A significant decrease in GSH levels and increases in MDA, eNOS, and 8-OHdG expressions were recorded. Additionally, CIS treatment had caused acidophilic staining in retinal histological appearance. ASTA treatment reduced the increases in MDA, eNOS, and 8-OHdG levels following CIS administration and increased the levels of GSH expressions, as well. Conclusions: These results may suggest that the ASTA molecule as a promising option to prevent retinal toxicity in patients receiving CIS treatment for malignant tumors.
    Link: Source
    Citations: