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      The antioxidative property of melatonin against brain ischemia

      Author(s): , , ,
      Publication date Created:
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      Journal: Expert Review of Neurotherapeutics
      Publisher: Informa UK Limited

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          Abstract

          This review briefly summarizes some of the large amount of data documenting the ability of melatonin to limit molecular and organ tissue damage in neural ischemia-reperfusion injury (stroke), where free radicals are generally considered as being responsible for much of the resulting tissue destruction.

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          Most cited references68

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          Viability thresholds and the penumbra of focal ischemia.

          K Hossmann (1994)
          The classic concept of the viability thresholds of ischemia differentiates between two critical flow rates, the threshold of electrical failure and the threshold of membrane failure. These thresholds mark the upper and lower flow limits of the ischemic penumbra which is thought to suffer only functional but not structural injury. Recent studies of the functional and metabolic disturbances suggest a more complex pattern of thresholds. At declining flow rates, protein synthesis is inhibited at first (at a threshold of about 0.55 ml/gm/min), followed by a stimulation of anaerobic glycolysis (at 0.35 ml/gm/min), the release of neurotransmitters and the beginning disturbance of energy metabolism (at about 0.20 ml/min), and finally the anoxic depolarization (< 0.15 ml/gm/min). The penumbra, as defined by the classic flow thresholds, does not remain viable for extended periods. Since viability of the tissue requires maintenance of energy-dependent metabolic processes, penumbra is redefined as a region of constrained blood supply in which the energy metabolism is preserved. Imaging of the penumbra by combining autoradiographic cerebral blood flow measurements with bioluminescent images of adenosine triphosphate (ATP) demonstrates a gradual expansion of the infarct core (in which ATP is depleted) into the penumbra until, after a few hours, the penumbra has disappeared. It is suggested that the limited survival of the penumbra is due to periinfarct depolarizations, which result in repeated episodes of tissue hypoxia, because the increased metabolic workload is not coupled to an adequate increase of collateral blood supply. This explains pharmacological suppression of periinfarct depolarizations lowering the threshold of metabolic disturbances and reducing the volume of the ischemic infarct.
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            The role of melatonin in the cells of the innate immunity: a review.

            C Yanes, R Calvo, Eliana M. Maldonado (2013)
            Melatonin is the major secretory product synthesized and secreted by the pineal gland and shows both a wide distribution within phylogenetically distant organisms from bacteria to humans and a great functional versatility. In recent years, a considerable amount of experimental evidence has accumulated showing a relationship between the nervous, endocrine, and immune systems. The molecular basis of the communication between these systems is the use of a common chemical language. In this framework, currently melatonin is considered one of the members of the neuroendocrine-immunological network. A number of in vivo and in vitro studies have documented that melatonin plays a fundamental role in neuroimmunomodulation. Based on the information published, it is clear that the majority of the present data in the literature relate to lymphocytes; thus, they have been rather thoroughly investigated, and several reviews have been published related to the mechanisms of action and the effects of melatonin on lymphocytes. However, few studies concerning the effects of melatonin on cells belonging to the innate immunity have been reported. Innate immunity provides the early line of defense against microbes and consists of both cellular and biochemical mechanisms. In this review, we have focused on the role of melatonin in the innate immunity. More specifically, we summarize the effects and action mechanisms of melatonin in the different cells that belong to or participate in the innate immunity, such as monocytes-macrophages, dendritic cells, neutrophils, eosinophils, basophils, mast cells, and natural killer cells. © 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.
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              A review of the multiple actions of melatonin on the immune system.

              Antonio Carrillo-Vico, Juan M. Guerrero, Patricia J. Lardone … (2005)
              This review summarizes the numerous observations published in recent years which have shown that one of the most significant of melatonin's pleiotropic effects is the regulation of the immune system. The overview summarizes the immune effects of pinealectomy and the association between rhythmic melatonin production and adjustments in the immune system as markers of melatonin's immunomodulatory actions. The effects of both in vivo and in vitromelatonin administration on non-specific, humoral, and cellular immune responses as well as on cellular proliferation and immune mediator production are presented. One of the main features that distinguishes melatonin from the classical hormones is its synthesis by a number of non-endocrine extrapineal organs, including the immune system. Herein, we summarize the presence of immune system-synthesized melatonin, its direct immunomodulatory effects on cytokine production, and its masking effects on exogenous melatonin action. The mechanisms of action of melatonin in the immune system are also discussed, focusing attention on the presence of membrane and nuclear receptors and the characterization of several physiological roles mediated by some receptor analogs in immune cells. The review focuses on melatonin's actions in several immune pathologies including infection, inflammation, and autoimmunity together with the relation between melatonin, immunity, and cancer.
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                Author and article information

                Journal
                Title: Expert Review of Neurotherapeutics
                Abbreviated Title: Expert Review of Neurotherapeutics
                Publisher: Informa UK Limited
                ISSN (Print): 1473-7175
                ISSN (Electronic): 1744-8360
                Publication date Created: May 06 2016
                Publication date Created: July 02 2016
                Publication date (Electronic): May 09 2016
                Publication date (Print): July 02 2016
                Volume: 16
                Issue: 7
                Pages: 841-848
                Article
                DOI: 10.1080/14737175.2016.1182020
                PubMed ID: 27108742
                SO-VID: ab01df3e-9088-4e02-b58f-1a6fd945e168
                Copyright © © 2016
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