Melatonin Metabolism and Aging

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: 15 June 2024 | Viewed by 1744

Special Issue Editor

Institute of Anatomy and Cell Biology, Medical Faculty of Martin Luther University Halle-Wittenberg, 06108 Halle (Saale), Germany
Interests: pancreatic islet; insulin; glucagon; somatostatin; melatonin receptor; glucose transporter; natural killer cells; pancreatic ductal adenocarcinoma; fatty liver; glucose metabolism

Special Issue Information

Dear Colleagues,

Melatonin is an important hormone of the circadian system and is centrally synthesized in vertebrates' pineal gland during the night. Aside from that, local synthesis is also described in several tissues and cells (e.g., retina, gut, immune cells). In the pineal gland, tryptophan is converted to melatonin via various intermediate stages, whereby the arylalkylamine N-acetyltransferase represents the key enzyme. Melatonin is widely known as a pleiotropic and universal antioxidant molecule, which regulates many physiological functions, e.g., the sleep–wake cycle, redox homeostasis, lipid and glucose metabolism and it additionally plays a role in the immune system. The effects of melatonin are indirectly mediated via melatonin receptors, which are found in most mammalian tissues. Another possibility is the direct transmission through interaction with intracellular components. Enzymatic melatonin degradation mainly occurs in the liver, mediated by the major enzyme cytochrome P450. Additionally, melatonin can be metabolized by other enzymatic, non-enzymatic, or free radical interactive processes. Reduction in melatonin secretion, especially decreased melatonin plasma levels, is increasingly discussed in association with aging and age-related diseases.

This Special Issue should provide further insights and knowledge about molecular signaling and cellular mechanisms underlying melatonin function as well as components involved in mammalian cells' melatonin metabolism. In this context, the influence of aging or age-related diseases should be particularly considered.

Dr. Ivonne Bazwinsky-Wutschke 
Guest Editor

Manuscript Submission Information

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Published Papers (1 paper)

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Review

44 pages, 4422 KiB  
Review
Non-Excitatory Amino Acids, Melatonin, and Free Radicals: Examining the Role in Stroke and Aging
by Victoria Jiménez Carretero, Eva Ramos, Pedro Segura-Chama, Adan Hernández, Andrés M Baraibar, Iris Álvarez-Merz, Francisco López Muñoz, Javier Egea, José M. Solís, Alejandro Romero and Jesús M. Hernández-Guijo
Antioxidants 2023, 12(10), 1844; https://doi.org/10.3390/antiox12101844 - 10 Oct 2023
Cited by 1 | Viewed by 1447
Abstract
The aim of this review is to explore the relationship between melatonin, free radicals, and non-excitatory amino acids, and their role in stroke and aging. Melatonin has garnered significant attention in recent years due to its diverse physiological functions and potential therapeutic benefits [...] Read more.
The aim of this review is to explore the relationship between melatonin, free radicals, and non-excitatory amino acids, and their role in stroke and aging. Melatonin has garnered significant attention in recent years due to its diverse physiological functions and potential therapeutic benefits by reducing oxidative stress, inflammation, and apoptosis. Melatonin has been found to mitigate ischemic brain damage caused by stroke. By scavenging free radicals and reducing oxidative damage, melatonin may help slow down the aging process and protect against age-related cognitive decline. Additionally, non-excitatory amino acids have been shown to possess neuroprotective properties, including antioxidant and anti-inflammatory in stroke and aging-related conditions. They can attenuate oxidative stress, modulate calcium homeostasis, and inhibit apoptosis, thereby safeguarding neurons against damage induced by stroke and aging processes. The intracellular accumulation of certain non-excitatory amino acids could promote harmful effects during hypoxia-ischemia episodes and thus, the blockade of the amino acid transporters involved in the process could be an alternative therapeutic strategy to reduce ischemic damage. On the other hand, the accumulation of free radicals, specifically mitochondrial reactive oxygen and nitrogen species, accelerates cellular senescence and contributes to age-related decline. Recent research suggests a complex interplay between melatonin, free radicals, and non-excitatory amino acids in stroke and aging. The neuroprotective actions of melatonin and non-excitatory amino acids converge on multiple pathways, including the regulation of calcium homeostasis, modulation of apoptosis, and reduction of inflammation. These mechanisms collectively contribute to the preservation of neuronal integrity and functions, making them promising targets for therapeutic interventions in stroke and age-related disorders. Full article
(This article belongs to the Special Issue Melatonin Metabolism and Aging)
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