Inhibitory Effect of Astaxanthin on Oxidative Stress-Induced Mitochondrial Dysfunction-A Mini-Review

Kim, Suhn Hyung; Kim, Hye Young

doi:10.3390/nu10091137

Cited by 187 publications

(149 citation statements)

References 75 publications

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“…The effects of natural AX in humans have been reviewed in more than 20 publications over the last 10 years and include studies on antioxidation, hepatoprotection, eye function, skin health, immune response, inflammation, gastric ulcer, cardiovascular system, muscle endurance, cancer, central nervous system, male fertility, metabolic syndrome, diabetes, and mitochondrial dysfunction (Ekpe, Inaku, & Ekpe, ; Fakhri, Abbaszadeh, Dargahi, & Jorjani, ; Fassett et al, , Fassett & Coombes, ; Galasso et al, ; Visioli & Artaria, ; Brown, Gough, Deb, Sparks, & McNaughton, ; Capelli, Jenkins, & Cysewski, ; Davinelli, Nielsen, & Scapagnini, ; Kim & Kim, ; Yamashita, ).…”

Section: Resultsmentioning

confidence: 99%

“…Abbreviations: ACNFP, Advisory Committee on Novel Foods and Processes; FSAI, Food Safety Authority of Ireland; NFA, National Food Administration. Fassett et al, 2008, Fassett & Coombes, 2012Galasso et al, 2018;Visioli & Artaria, 2017;Brown, Gough, Deb, Sparks, & McNaughton, 2018;Capelli, Jenkins, & Cysewski, 2013;Davinelli, Nielsen, & Scapagnini, 2018;Kim & Kim, 2018;.…”

Section: Clinical Safety Of Natural Axmentioning

confidence: 99%

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Astaxanthin: How much is too much? A safety review

Brendler

Williamson

2019

Phytotherapy Research

100

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Astaxanthin (AX)‐containing preparations are increasingly popular as health food supplements. Evaluating the maximum safe daily intake of AX is important when setting dose levels for these products and currently, there are discrepancies in recommendations by different regulatory authorities. We have therefore conducted a review of approved dose levels, clinical trials of natural AX, and toxicological studies with natural and synthetic AX. Recommended or approved doses varied in different countries and ranged between 2 and 24 mg. We reviewed 87 human studies, none of which found safety concerns with natural AX supplementation, 35 with doses ≥12 mg/day. An acceptable daily intake (ADI) of 2 mg as recently proposed by European Food Safety Authority was based on a toxicological study in rats using synthetic AX. However, synthetically produced AX is chemically different from natural AX, so results with synthetic AX should not be used in assessing natural AX safety. In addition, few safety studies have been conducted in either humans or animals with synthetic AX. We therefore recommend the ADI for natural AX to be based only on studies conducted with natural AX and further studies to be conducted with synthetic AX (including human clinical trials) to establish a separate ADI for synthetic AX.

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Section: Resultsmentioning

confidence: 99%

Section: Clinical Safety Of Natural Axmentioning

confidence: 99%

Astaxanthin: How much is too much? A safety review

Brendler

Williamson

2019

Phytotherapy Research

100

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“…Astaxanthin (3,30-dihydroxy-β, β-carotene-4,40-dione) is a red pigment belonging to the sub-class of xanthophyllic carotenoids; it is found mainly in microalgae, mushrooms, and complex plants, as well as in salmon, trout, and crustacean cells [114]. Astaxanthin shows strong antioxidative properties and can neutralize singlet oxygen and free radicals, thus, preventing lipid peroxidation [173]. Its properties are due to the presence of numerous conjugated multiple bonds.…”

Section: Vitamins and Provitaminsmentioning

confidence: 99%

“…Its properties are due to the presence of numerous conjugated multiple bonds. It has been demonstrated that the most important effects of astaxanthin's activity include the prevention of neuron damage and inhibition of cell membrane peroxidation [173]. Astaxanthin is composed of a long, nonpolar, conjugated bond connecting polar ion rings located on both ends of the chain.…”

Section: Vitamins and Provitaminsmentioning

confidence: 99%

The Role of Dietary Antioxidants in the Pathogenesis of Neurodegenerative Diseases and Their Impact on Cerebral Oxidoreductive Balance

et al. 2020

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Neurodegenerative diseases are progressive diseases of the nervous system that lead to neuron loss or functional disorders. Neurodegenerative diseases require long-term, sometimes life-long pharmacological treatment, which increases the risk of adverse effects and a negative impact of pharmaceuticals on the patients' general condition. One of the main problems related to the treatment of this type of condition is the limited ability to deliver drugs to the brain due to their poor solubility, low bioavailability, and the effects of the blood-brain barrier. Given the above, one of the main objectives of contemporary scientific research focuses on the prevention of neurodegenerative diseases. As disorders related to the competence of the antioxidative system are a marker in all diseases of this type, the primary prophylactics should entail the use of exogenous antioxidants, particularly ones that can be used over extended periods, regardless of the patient's age, and that are easily available, e.g., as part of a diet or as diet supplements. The paper analyzes the significance of the oxidoreductive balance in the pathogenesis of neurodegenerative diseases. Based on information published globally in the last 10 years, an analysis is also provided with regard to the impact of exogenous antioxidants on brain functions with respect to the prevention of this type of diseases.

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“…ATX, with its superior anti-oxidant and anti-inflammatory properties, exhibits protective effects in cardiovascular health and disease, ischemia and reperfusion injury, cognitive function with age, and neurodegeneration [16]. However, its use in the food, feed, and pharmaceutical fields is limited, owing to low bioavailability, poor stability during thermochemical treatments, susceptibility to oxidation, and poor organoleptic characteristics.…”

Section: Discussionmentioning

confidence: 99%

Astaxanthin-loaded polymer-lipid hybrid nanoparticles (ATX-LPN): assessment of potential otoprotective effects

Chen

Tong

et al. 2020

J Nanobiotechnol

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Background: Ototoxicity is one of the major side effects of platinum-based chemotherapy, especially cisplatin therapy. To date, no FDA approved agents to alleviate or prevent this ototoxicity are available. However, ototoxicity is generally believed to be produced by excessive generation of reactive oxygen species (ROS) in the inner ear, thus leading to the development of various antioxidants, which act as otoprotective agents. Astaxanthin (ATX) is an interesting candidate in the development of new therapies for preventing and treating oxidative stress-related pathologies, owing to its unique antioxidant capacity. Methods and results:In this study, we aimed to evaluate the potential antioxidant properties of ATX in the inner ear by using the HEI-OC1 cell line, zebrafish, and guinea pigs. Because ATX has poor solubility and cannot pass through round window membranes (RWM), we established lipid-polymer hybrid nanoparticles (LPN) for loading ATX. The LPN enabled ATX to penetrate RWM and maintain concentrations in the perilymph in the inner ear for 24 h after a single injection. ATX-LPN were found to have favorable biocompatibility and to strongly affect cisplatin-induced generation of ROS, on the basis of DCFHDA staining in HEI-OC1 cells. JC-1 and MitoTracker Green staining suggested that ATX-LPN successfully reversed the decrease in mitochondrial membrane potential induced by cisplatin in vitro and rescued cells from early stages of apoptosis, as demonstrated by FACS stained with Annexin V-FITC/PI. Moreover, ATX-LPN successfully attenuated OHC losses in cultured organ of Corti and animal models (zebrafish and guinea pigs) in vivo. In investigating the protective mechanism of ATX-LPN, we found that ATX-LPN decreased the expression of pro-apoptotic proteins (caspase 3/9 and cytochrome-c) and increased expression of the anti-apoptotic protein Bcl-2. In addition, the activation of JNK induced by CDDP was up-regulated and then decreased after the administration of ATX-LPN, while P38 stayed unchanged. Conclusions:To best of our knowledge, this is first study concluded that ATX-LPN as a new therapeutic agent for the prevention of cisplatin-induced ototoxicity.

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Inhibitory Effect of Astaxanthin on Oxidative Stress-Induced Mitochondrial Dysfunction-A Mini-Review

Cited by 187 publications

References 75 publications

Astaxanthin: How much is too much? A safety review

Astaxanthin: How much is too much? A safety review

The Role of Dietary Antioxidants in the Pathogenesis of Neurodegenerative Diseases and Their Impact on Cerebral Oxidoreductive Balance

Astaxanthin-loaded polymer-lipid hybrid nanoparticles (ATX-LPN): assessment of potential otoprotective effects

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