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      On the Neuroprotective Role of Astaxanthin: New Perspectives?

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          Abstract

          Astaxanthin is a carotenoid with powerful antioxidant and anti-inflammatory activity produced by several freshwater and marine microorganisms, including bacteria, yeast, fungi, and microalgae. Due to its deep red-orange color it confers a reddish hue to the flesh of salmon, shrimps, lobsters, and crayfish that feed on astaxanthin-producing organisms, which helps protect their immune system and increase their fertility. From the nutritional point of view, astaxanthin is considered one of the strongest antioxidants in nature, due to its high scavenging potential of free radicals in the human body. Recently, astaxanthin is also receiving attention for its effect on the prevention or co-treatment of neurological pathologies, including Alzheimer and Parkinson diseases. In this review, we focus on the neuroprotective properties of astaxanthin and explore the underlying mechanisms to counteract neurological diseases, mainly based on its capability to cross the blood-brain barrier and its oxidative, anti-inflammatory, and anti-apoptotic properties.

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          Superoxide radical and superoxide dismutases.

          I Fridovich (1995)
          O2- oxidizes the [4Fe-4S] clusters of dehydratases, such as aconitase, causing-inactivation and release of Fe(II), which may then reduce H2O2 to OH- +OH.. SODs inhibit such HO. production by scavengingO2-, but Cu, ZnSODs, by virtue of a nonspecific peroxidase activity, may peroxidize spin trapping agents and thus give the appearance of catalyzing OH. production from H2O2. There is a glycosylated, tetrameric Cu, ZnSOD in the extracellular space that binds to acidic glycosamino-glycans. It minimizes the reaction of O2- with NO. E. coli, and other gram negative microorganisms, contain a periplasmic Cu, ZnSOD that may serve to protect against extracellular O2-. Mn(III) complexes of multidentate macrocyclic nitrogenous ligands catalyze the dismutation of O2- and are being explored as potential pharmaceutical agents. SOD-null mutants have been prepared to reveal the biological effects of O2-. SodA, sodB E. coli exhibit dioxygen-dependent auxotrophies and enhanced mutagenesis, reflecting O2(-)-sensitive biosynthetic pathways and DNA damage. Yeast, lacking either Cu, ZnSOD or MnSOD, are oxygen intolerant, and the double mutant was hypermutable and defective in sporulation and exhibited requirements for methionine and lysine. A Cu, ZnSOD-null Drosophila exhibited a shortened lifespan.
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            Inflammation in neurodegenerative disease--a double-edged sword.

            Tony Wyss-Coray, Lennart Mucke (2002)
            Inflammation is a defense reaction against diverse insults, designed to remove noxious agents and to inhibit their detrimental effects. It consists of a dazzling array of molecular and cellular mechanisms and an intricate network of controls to keep them in check. In neurodegenerative diseases, inflammation may be triggered by the accumulation of proteins with abnormal conformations or by signals emanating from injured neurons. Given the multiple functions of many inflammatory factors, it has been difficult to pinpoint their roles in specific (patho)physiological situations. Studies of genetically modified mice and of molecular pathways in activated glia are beginning to shed light on this issue. Altered expression of different inflammatory factors can either promote or counteract neurodegenerative processes. Since many inflammatory responses are beneficial, directing and instructing the inflammatory machinery may be a better therapeutic objective than suppressing it.
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              GAP-43: an intrinsic determinant of neuronal development and plasticity.

              Larry I. Benowitz, Aryeh Routtenberg (1997)
              Several lines of investigation have helped clarify the role of GAP-43 (FI, B-50 or neuromodulin) in regulating the growth state of axon terminals. In transgenic mice, overexpression of GAP-43 leads to the spontaneous formation of new synapses and enhanced sprouting after injury. Null mutation of the GAP-43 gene disrupts axonal pathfinding and is generally lethal shortly after birth. Manipulations of GAP-43 expression likewise have profound effects on neurite outgrowth for cells in culture. GAP-43 appears to be involved in transducing intra- and extracellular signals to regulate cytoskeletal organization in the nerve ending. Phosphorylation by protein kinase C is particularly significant in this regard, and is linked with both nerve-terminal sprouting and long-term potentiation. In the brains of humans and other primates, high levels of GAP-43 persist in neocortical association areas and in the limbic system throughout life, where the protein might play an important role in mediating experience-dependent plasticity.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Mar Drugs
                Journal ID (iso-abbrev): Mar Drugs
                Journal ID (publisher-id): marinedrugs
                Title: Marine Drugs
                Publisher: MDPI
                ISSN (Electronic): 1660-3397
                Publication date (Electronic): 24 July 2018
                Publication date Collection: August 2018
                Volume: 16
                Issue: 8
                Electronic Location Identifier: 247
                Affiliations
                [1 ]Department of Marine Biotechnology, Stazione Zoologica Anton Dohrn, Villa Comunale, 80121 Naples, Italy; christian.galasso@ 123456szn.it (C.G.); ida.orefice@ 123456szn.it (I.O.); paola.pellone@ 123456gmail.com (P.P.); robertamiele90@ 123456libero.it (R.M.); adrianna.ianora@ 123456szn.it (A.I.)
                [2 ]Department of Research Infrastructures for Marine Biological Resources, Stazione Zoologica Anton Dohrn, Villa Comunale, 80121 Naples, Italy; paola.cirino@ 123456szn.it
                Author notes
                [* ]Correspondence: christophe.brunet@ 123456szn.it (C.B.); clementina.sansone@ 123456szn.it (C.S.); Tel.: +39-081-583-3603 (C.B.); +39-081-583-3221 (C.S.)
                Author information
                https://orcid.org/0000-0002-0688-4199
                Article
                Publisher ID: marinedrugs-16-00247
                DOI: 10.3390/md16080247
                PMC ID: 6117702
                PubMed ID: 30042358
                SO-VID: 5581d91b-6df3-46a5-8016-45d0ba564f39
                Copyright © © 2018 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 11 July 2018
                Date accepted : 23 July 2018
                Categories
                Subject: Review

                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: astaxanthin,neuroinflammation,neuroprotective effect,neuroactive carotenoids,neurodegenerative diseases
                Data availability:
                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: astaxanthin, neuroinflammation, neuroprotective effect, neuroactive carotenoids, neurodegenerative diseases

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