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Special Issue "Melatonin and Redox Signaling"
A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".
Deadline for manuscript submissions: 31 March 2020.
Melatonin has a broad spectrum of physiological effects in the entire animal kingdom, from unicellular organisms to higher vertebrates. The pineal gland is one of the various organs in which melatonin is produced. The main regulator of melatonin secretion by the vertebrate pineal gland is the light–dark cycle. Thus, during the day, human serum melatonin concentrations are low (5–20 pg/mL), while at night, blood levels reach peak values (80–150 pg/mL). By contrast, the melatonin produced in peripheral tissues seems to have intracrine, autocrine, and paracrine roles as it does not enter circulation.
Studies during the last 25 years have documented both receptor-mediated and receptor-independent actions of melatonin. This indoleamine acts by binding to membrane and nuclear receptors, by interacting with cytosolic proteins, and as a powerful free radical scavenger. Melatonin is especially effective as an antioxidant because it utilizes a wide variety of means to reduce oxidative stress. Firstly, melatonin scavenges several toxic reactants, including the highly toxic hydroxyl radical, and perhaps even more importantly, it takes advantage of its derivatives, which also are efficient free radical scavengers. Secondly, this indoleamine also functions as an indirect antioxidant because of its ability to stimulate the expression and activity of antioxidant enzymes which remove free radicals and their precursors. One additional important feature of melatonin’s ability to reduce oxidative stress is that melatonin is a mitochondria-targeted antioxidant. Several studies have provided evidence that melatonin could protect mitochondria from oxidative stress resulting from different toxins. Moreover, it has been shown that melatonin upregulates the activity of all four complexes in the electron transport chain, preserves the mitochondrial membrane potential, increases the activity of mitochondrial uncoupling proteins, enhances mitophagy, and improves mitochondrial biogenesis
This Special Issue aims to publish original research papers and reviews on melatonin and its relationships with oxidative stress and redox signaling pathways, and wishes to be an instrument for communication and dissemination of the most recent findings about the beneficial therapeutic implications of this indoleamine in human diseases.
Prof. Dr. Joaquín J. García
Prof. Darío Acuña-Castroviejo
Manuscript Submission Information
Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.
Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.
Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1400 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.
- oxidative stress
- redox signaling
- lipid and protein oxidation
- mitochondrial dysfunction
- therapeutic implications in human diseases