Journal articles: 'Melatonin – Pathophysiology'

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Hardeland, Rüdiger. "Neurobiology, Pathophysiology, and Treatment of Melatonin Deficiency and Dysfunction." Scientific World Journal 2012 (2012): 1–18. http://dx.doi.org/10.1100/2012/640389.

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Melatonin is a highly pleiotropic signaling molecule, which is released as a hormone of the pineal gland predominantly during night. Melatonin secretion decreases during aging. Reduced melatonin levels are also observed in various diseases, such as types of dementia, some mood disorders, severe pain, cancer, and diabetes type 2. Melatonin dysfunction is frequently related to deviations in amplitudes, phasing, and coupling of circadian rhythms. Gene polymorphisms of melatonin receptors and circadian oscillator proteins bear risks for several of the diseases mentioned. A common symptom of insufficient melatonin signaling is sleep disturbances. It is necessary to distinguish between symptoms that are curable by short melatonergic actions and others that require extended actions during night. Melatonin immediate release is already effective, at moderate doses, for reducing difficulties of falling asleep or improving symptoms associated with poorly coupled circadian rhythms, including seasonal affective and bipolar disorders. For purposes of a replacement therapy based on longer-lasting melatonergic actions, melatonin prolonged release and synthetic agonists have been developed. Therapies with melatonin or synthetic melatonergic drugs have to consider that these agents do not only act on the SCN, but also on numerous organs and cells in which melatonin receptors are also expressed.

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Konenkov, Vladimir Iosifovich, Vadim Valerievich Klimontov, Svetlana Viktorovna Michurina, M. A. Prudnikova, and I. Ju Ishenko. "Melatonin and diabetes: from pathophysiology to the treatment perspectives." Diabetes mellitus 16, no. 2 (June 15, 2013): 11–16. http://dx.doi.org/10.14341/2072-0351-3751.

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Pineal hormone melatonin synchronizes insulin secretion and glucose homeostasis with solar periods. Misalliance between melatonin-mediated circadian rhythms and insulin secretion characterizes diabetes mellitus type 1 (T1DM) and type 2 (T2DM). Insulin deficiency in T1DM is accompanied by increased melatonin production. Conversely, T2DM is characterized by diminished melatonin secretion. In genome-wide association studies the variants of melatonin receptor MT2 gene (rs1387153 and rs10830963) were associated with fasting glucose, beta-cell function and T2DM. In experimental models of diabetes melatonin enhanced beta-cell proliferation and neogenesis, improved insulin resistance and alleviated oxidative stress in retina and kidneys. However, further investigation is required to assess the therapeutic value of melatonin in diabetic patients.

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Maltsev, S. V., and L. A. Itkina. "Physiology and pathophysiology of melatonin." Kazan medical journal 80, no. 5 (September 15, 1999): 390–93. http://dx.doi.org/10.17816/kazmj70226.

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Studies devoted to the role of biogenic monoamines and peptide hormones in the formation of physiological and pathophysiological reactions have attracted particular attention in recent years. At the same time, the important role of the cells producing these substances, united by Peasse into a single functionally active peripheral neuroendocrine system (APU D-system), is emphasized.

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Lee, Jung Goo, Young Sup Woo, Sung Woo Park, Dae-Hyun Seog, Mi Kyoung Seo, and Won-Myong Bahk. "The Neuroprotective Effects of Melatonin: Possible Role in the Pathophysiology of Neuropsychiatric Disease." Brain Sciences 9, no. 10 (October 21, 2019): 285. http://dx.doi.org/10.3390/brainsci9100285.

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Melatonin is a hormone that is secreted by the pineal gland. To date, melatonin is known to regulate the sleep cycle by controlling the circadian rhythm. However, recent advances in neuroscience and molecular biology have led to the discovery of new actions and effects of melatonin. In recent studies, melatonin was shown to have antioxidant activity and, possibly, to affect the development of Alzheimer’s disease (AD). In addition, melatonin has neuroprotective effects and affects neuroplasticity, thus indicating potential antidepressant properties. In the present review, the new functions of melatonin are summarized and a therapeutic target for the development of new drugs based on the mechanism of action of melatonin is proposed.

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Peres, MFP. "Melatonin, the Pineal Gland and their Implications for Headache Disorders." Cephalalgia 25, no. 6 (June 2005): 403–11. http://dx.doi.org/10.1111/j.1468-2982.2005.00889.x.

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There is now evidence that melatonin may have a role in the biological regulation of circadian rhythms, sleep, mood, and ageing. Altered melatonin levels in cluster headache and migraine have been documented. Melatonin mechanisms are related to headache pathophysiology in many ways, including its anti-inflammatory effect, toxic free radical scavenging, reduction of proinflammatory cytokine up-regulation, nitric oxide synthase activity and dopamine release inhibition, membrane stabilization, GABA and opioid analgesia potentiation, glutamate neurotoxicity protection, neurovascular regulation, serotonin modulation, and the similarity of chemical structure to that of indomethacin. Treatment of headache disorders with melatonin and other chronobiotic agents is promising. A doubleblind, placebo-controlled trial shows melatonin is effective in cluster headache prevention, other studies also show benefit in other disorders. Melatonin plays an important role in headache disorders, offering new avenues for studying their pathophysiology and treatment.

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Reiter, Russel J. "Melatonin and the pathophysiology of cellular membranes." MARMARA PHARMACEUTCAL JOURNAL 1, no. 14 (January 1, 2010): 1–9. http://dx.doi.org/10.12991/201014457.

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Claustrat, Bruno, Jocelyne Brun, and Guy Chazot. "The basic physiology and pathophysiology of melatonin." Sleep Medicine Reviews 9, no. 1 (February 2005): 11–24. http://dx.doi.org/10.1016/j.smrv.2004.08.001.

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Anderson, George, Moses Rodriguez, and Russel J. Reiter. "Multiple Sclerosis: Melatonin, Orexin, and Ceramide Interact with Platelet Activation Coagulation Factors and Gut-Microbiome-Derived Butyrate in the Circadian Dysregulation of Mitochondria in Glia and Immune Cells." International Journal of Molecular Sciences 20, no. 21 (November 5, 2019): 5500. http://dx.doi.org/10.3390/ijms20215500.

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Recent data highlight the important roles of the gut microbiome, gut permeability, and alterations in mitochondria functioning in the pathophysiology of multiple sclerosis (MS). This article reviews such data, indicating two important aspects of alterations in the gut in the modulation of mitochondria: (1) Gut permeability increases toll-like receptor (TLR) activators, viz circulating lipopolysaccharide (LPS), and exosomal high-mobility group box (HMGB)1. LPS and HMGB1 increase inducible nitric oxide synthase and superoxide, leading to peroxynitrite-driven acidic sphingomyelinase and ceramide. Ceramide is a major driver of MS pathophysiology via its impacts on glia mitochondria functioning; (2) Gut dysbiosis lowers production of the short-chain fatty acid, butyrate. Butyrate is a significant positive regulator of mitochondrial function, as well as suppressing the levels and effects of ceramide. Ceramide acts to suppress the circadian optimizers of mitochondria functioning, viz daytime orexin and night-time melatonin. Orexin, melatonin, and butyrate increase mitochondria oxidative phosphorylation partly via the disinhibition of the pyruvate dehydrogenase complex, leading to an increase in acetyl-coenzyme A (CoA). Acetyl-CoA is a necessary co-substrate for activation of the mitochondria melatonergic pathway, allowing melatonin to optimize mitochondrial function. Data would indicate that gut-driven alterations in ceramide and mitochondrial function, particularly in glia and immune cells, underpin MS pathophysiology. Aryl hydrocarbon receptor (AhR) activators, such as stress-induced kynurenine and air pollutants, may interact with the mitochondrial melatonergic pathway via AhR-induced cytochrome P450 (CYP)1b1, which backward converts melatonin to N-acetylserotonin (NAS). The loss of mitochnodria melatonin coupled with increased NAS has implications for altered mitochondrial function in many cell types that are relevant to MS pathophysiology. NAS is increased in secondary progressive MS, indicating a role for changes in the mitochondria melatonergic pathway in the progression of MS symptomatology. This provides a framework for the integration of diverse bodies of data on MS pathophysiology, with a number of readily applicable treatment interventions, including the utilization of sodium butyrate.

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Mondes, Pedro Henrique de Lima, and Eduardo Koji Tamura. "Melatonina em Animais de Companhia: uma Revisão de Literatura." Ensaios e Ciência C Biológicas Agrárias e da Saúde 25, no. 5-esp (March 14, 2022): 671–81. http://dx.doi.org/10.17921/1415-6938.2021v25n5-espp671-681.

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A melatonina, N-acetil-5-metoxi-triptamina, é uma indolamina que possui diversas ações no organismo, desde regulação de ritmos circadianos, modulação do sistema imune, indutor do sono em determinas espécies e até eliminação de radicais livres. O objetivo desta revisão foi descrever o histórico, a síntese, os mecanismos de ação e os efeitos da melatonina, além de descrever trabalhos que utilizaram a melatonina em patologias associadas aos animais domésticos, em especial, nos cães e nos gatos. Esta revisão pode ser classificada como integrativa, com metodologia que consistiu em selecionar artigos das plataformas online como PubMed e Google Acadêmico, com a combinação de palavras-chave como “melatonin”, “dog”, “cat”, “circadian”, “rhythm”, “mammals”, desde que investigassem o envolvimento da indolamina na fisiopatologia de animais de companhia, ou que utilizassem a melatonina como método terapêutico no campo da Medicina Veterinária. Os artigos escolhidos dataram de 1958 até 2020. Os resultados demonstraram efeitos diversos, em várias áreas de especializações da veterinária, entre essas, oncologia, oftalmologia, anestesiologia, reprodução, endocrinologia, neurologia, dermatologia e gastroenterologia. Apesar dos resultados obtidos, a melatonina ainda é pouco estudada em trabalhos clínicos e científicos veterinários e, por isso, necessita de mais investigação, uma vez que possui potencial terapêutico em muitas das enfermidades que acometem animais de companhia. Palavras-chave: Glândula Pineal. Medicina Veterinária. Cães. Gatos. Abstract Melatonin, N-acetyl-5-methoxy-tryptamine, is an indolamine that has various effects in the organism, from regulation of circadian rhythms to immune system modulation, sleep induction in some species and to scavenger of free radicals. This review aimed to described the history, action mechanisms and melatonin effects, in addition to, also describe studies focusing in therapeutic use of melatonin in pathologies associated with companion animals, specially dogs and cats. This review can be classified as integrative, with a methodology consisting of selected articles from online platforms, PubMed and Google Scholar, using the combination of keywords such as “melatonin”, “dog”, “cat”, “circadian”, “rhythm”, “mammals”, since they investigate the indolamine involvement in the companion animals pathophysiology, or that use melatonin as a therapeutic method in the Veterinary Medicine field. The selected articles were from 1958 to 2020. The results demonstrated different effects in some veterinary specialization areas, including oncology, ophthalmology, anesthesiology, reproduction, endocrinology, neurology, dermatology and gastroenterology. Despite the results obtained, melatonin is still poorly studied in clinical and scientific veterinary and, therefore, needs further investigation, since it has therapeutic potential in many diseases that affect companion animals. Keywords: Pineal Gland. Veterinary Medicine. Dogs. Cats.

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Mondes, Pedro Henrique de Lima, and Eduardo Koji Tamura. "Melatonina em Animais de Companhia: uma Revisão de Literatura." Ensaios e Ciência C Biológicas Agrárias e da Saúde 25, no. 5-esp. (March 14, 2022): 671–81. http://dx.doi.org/10.17921/1415-6938.2021v25n5-esp.p671-681.

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A melatonina, N-acetil-5-metoxi-triptamina, é uma indolamina que possui diversas ações no organismo, desde regulação de ritmos circadianos, modulação do sistema imune, indutor do sono em determinas espécies e até eliminação de radicais livres. O objetivo desta revisão foi descrever o histórico, a síntese, os mecanismos de ação e os efeitos da melatonina, além de descrever trabalhos que utilizaram a melatonina em patologias associadas aos animais domésticos, em especial, nos cães e nos gatos. Esta revisão pode ser classificada como integrativa, com metodologia que consistiu em selecionar artigos das plataformas online como PubMed e Google Acadêmico, com a combinação de palavras-chave como “melatonin”, “dog”, “cat”, “circadian”, “rhythm”, “mammals”, desde que investigassem o envolvimento da indolamina na fisiopatologia de animais de companhia, ou que utilizassem a melatonina como método terapêutico no campo da Medicina Veterinária. Os artigos escolhidos dataram de 1958 até 2020. Os resultados demonstraram efeitos diversos, em várias áreas de especializações da veterinária, entre essas, oncologia, oftalmologia, anestesiologia, reprodução, endocrinologia, neurologia, dermatologia e gastroenterologia. Apesar dos resultados obtidos, a melatonina ainda é pouco estudada em trabalhos clínicos e científicos veterinários e, por isso, necessita de mais investigação, uma vez que possui potencial terapêutico em muitas das enfermidades que acometem animais de companhia. Palavras-chave: Glândula Pineal. Medicina Veterinária. Cães. Gatos. Abstract Melatonin, N-acetyl-5-methoxy-tryptamine, is an indolamine that has various effects in the organism, from regulation of circadian rhythms to immune system modulation, sleep induction in some species and to scavenger of free radicals. This review aimed to described the history, action mechanisms and melatonin effects, in addition to, also describe studies focusing in therapeutic use of melatonin in pathologies associated with companion animals, specially dogs and cats. This review can be classified as integrative, with a methodology consisting of selected articles from online platforms, PubMed and Google Scholar, using the combination of keywords such as “melatonin”, “dog”, “cat”, “circadian”, “rhythm”, “mammals”, since they investigate the indolamine involvement in the companion animals pathophysiology, or that use melatonin as a therapeutic method in the Veterinary Medicine field. The selected articles were from 1958 to 2020. The results demonstrated different effects in some veterinary specialization areas, including oncology, ophthalmology, anesthesiology, reproduction, endocrinology, neurology, dermatology and gastroenterology. Despite the results obtained, melatonin is still poorly studied in clinical and scientific veterinary and, therefore, needs further investigation, since it has therapeutic potential in many diseases that affect companion animals. Keywords: Pineal Gland. Veterinary Medicine. Dogs. Cats.

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Pandi-Perumal, Seithikurippu R., Ahmed S. BaHammam, Nwakile I. Ojike, Oluwaseun A. Akinseye, Tetyana Kendzerska, Kenneth Buttoo, Perundurai S. Dhandapany, Gregory M. Brown, and Daniel P. Cardinali. "Melatonin and Human Cardiovascular Disease." Journal of Cardiovascular Pharmacology and Therapeutics 22, no. 2 (July 27, 2016): 122–32. http://dx.doi.org/10.1177/1074248416660622.

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The possible therapeutic role of melatonin in the pathophysiology of coronary artery disorder (CAD) is increasingly being recognized. In humans, exogenous melatonin has been shown to decrease nocturnal hypertension, improve systolic and diastolic blood pressure, reduce the pulsatility index in the internal carotid artery, decrease platelet aggregation, and reduce serum catecholamine levels. Low circulating levels of melatonin are reported in individuals with CAD, arterial hypertension, and congestive heart failure. This review assesses current literature on the cardiovascular effects of melatonin in humans. It can be concluded that melatonin deserves to be considered in clinical trials evaluating novel therapeutic interventions for cardiovascular disorders.

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Vogler, Barbara, Alan M. Rapoport, Stewart J. Tepper, Fred Sheftell, and Marcelo E. Bigal. "Role of Melatonin in the Pathophysiology of Migraine." CNS Drugs 20, no. 5 (2006): 343–50. http://dx.doi.org/10.2165/00023210-200620050-00001.

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Reiter, Russel, Lei Tang, Joaquin J. Garcia, and Antonio Muñoz-Hoyos. "Pharmacological actions of melatonin in oxygen radical pathophysiology." Life Sciences 60, no. 25 (May 1997): 2255–71. http://dx.doi.org/10.1016/s0024-3205(97)00030-1.

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Wang, Ye-qing, Ya-jie Jiang, Man-shu Zou, Jian Liu, Hong-qing Zhao, and Yu-hong Wang. "Antidepressant actions of melatonin and melatonin receptor agonist: Focus on pathophysiology and treatment." Behavioural Brain Research 420 (February 2022): 113724. http://dx.doi.org/10.1016/j.bbr.2021.113724.

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Bekyarova, Ganka, Maria Tzaneva, Minka Hristova, and Krasimir Hristov. "Melatonin protection against burn-induced liver injury. A review." Open Medicine 9, no. 1 (February 1, 2014): 148–58. http://dx.doi.org/10.2478/s11536-013-0253-7.

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AbstractSevere thermal injury may be complicated by dysfunction of organs distant from the original burn wound, including the liver, and represents a serious clinical problem. Although pathophysiology of burn-induced liver injury remains unclear, increasing evidence implicate activation of inflammatory response, oxidative stress, endothelial dysfunction and microcirculatory disorders as the main mechanisms of hepatic injury. Several studies suggest melatonin as a multifunctional indolamine that counteracts some of the pathophysiologic steps and displays significant beneficial effects against burn-induced cellular injury. This review summarizes the role of melatonin in restricting the burn-induced hepatic injury and focuses on its effects on oxidative stress, inflammatory response, endothelial dysfunction and microcirculatory disorders as well as on signaling pathways such as regulation of nuclear erythroid 2-related factor 2 (Nrf2) and nuclear factor-kappaB (NF-kB). Further studies are necessary to elucidate the modulating effect of melatonin on the transcription factor responsible for the regulation of the pro-inflammatory and antioxidant genes involved in burn injuries.

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Repova, Kristina, Tomas Baka, Kristina Krajcirovicova, Peter Stanko, Silvia Aziriova, Russel J. Reiter, and Fedor Simko. "Melatonin as a Potential Approach to Anxiety Treatment." International Journal of Molecular Sciences 23, no. 24 (December 19, 2022): 16187. http://dx.doi.org/10.3390/ijms232416187.

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Anxiety disorders are the most common mental diseases. Anxiety and the associated physical symptoms may disturb social and occupational life and increase the risk of somatic diseases. The pathophysiology of anxiety development is complex and involves alterations in stress hormone production, neurosignaling pathways or free radical production. The various manifestations of anxiety, its complex pathophysiological background and the side effects of available treatments underlie the quest for constantly seeking therapies for these conditions. Melatonin, an indolamine produced in the pineal gland and released into the blood on a nightly basis, has been demonstrated to exert anxiolytic action in animal experiments and different clinical conditions. This hormone influences a number of physiological actions either via specific melatonin receptors or by receptor-independent pleiotropic effects. The underlying pathomechanism of melatonin’s benefit in anxiety may reside in its sympatholytic action, interaction with the renin–angiotensin and glucocorticoid systems, modulation of interneuronal signaling and its extraordinary antioxidant and radical scavenging nature. Of importance, the concentration of this indolamine is significantly higher in cerebrospinal fluid than in the blood. Thus, ensuring sufficient melatonin production by reducing light pollution, which suppresses melatonin levels, may represent an endogenous neuroprotective and anxiolytic treatment. Since melatonin is freely available, economically undemanding and has limited side effects, it may be considered an additional or alternative treatment for various conditions associated with anxiety.

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Anderson, George. "Integrating Pathophysiology in Migraine: Role of the Gut Microbiome and Melatonin." Current Pharmaceutical Design 25, no. 33 (November 19, 2019): 3550–62. http://dx.doi.org/10.2174/1381612825666190920114611.

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Background: The pathoetiology and pathophysiology of migraine are widely accepted as unknown. Methods: The current article reviews the wide array of data associated with the biological underpinnings of migraine and provides a framework that integrates previously disparate bodies of data. Results: The importance of alterations in stress- and pro-inflammatory cytokine- induced gut dysbiosis, especially butyrate production, are highlighted. This is linked to a decrease in the availability of melatonin, and a relative increase in the N-acetylserotonin/melatonin ratio, which has consequences for the heightened glutamatergic excitatory transmission in migraine. It is proposed that suboptimal mitochondria functioning and metabolic regulation drive alterations in astrocytes and satellite glial cells that underpin the vasoregulatory and nociceptive changes in migraine. Conclusion: This provides a framework not only for classical migraine associated factors, such as calcitonin-gene related peptide and serotonin, but also for wider factors in the developmental pathoetiology of migraine. A number of future research and treatment implications arise, including the clinical utilization of sodium butyrate and melatonin in the management of migraine.

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Peres, Mario FP, Marcelo M. Valença, Fernanda G. Amaral, and José Cipolla-Neto. "Current understanding of pineal gland structure and function in headache." Cephalalgia 39, no. 13 (August 1, 2019): 1700–1709. http://dx.doi.org/10.1177/0333102419868187.

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Purpose The pineal gland plays an important role in biological rhythms, circadian and circannual variations, which are key aspects in several headache disorders. Overview Melatonin, the main pineal secreting hormone, has been extensively studied in primary and secondary headache disorders. Altered melatonin secretion occurs in many headache syndromes. Experimental data show pineal gland and melatonin both interfere in headache animal models, decreasing trigeminal activation. Melatonin has been shown to regulate CGRP and control its release. Discussion Melatonin has been used successfully as a treatment for migraine, cluster headaches and other headaches. There is a rationale for including the pineal gland as a relevant brain structure in the mechanisms of headache pathophysiology, and melatonin as a treatment option in primary headache.

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Srinivasan, Venkataramanujam, Yoshiji Ohta, Javier Espino, Jose A. Pariente, Ana B. Rodriguez, Mahaneem Mohamed, and Rahimah Zakaria. "Metabolic Syndrome, its Pathophysiology and the Role of Melatonin." Recent Patents on Endocrine, Metabolic & Immune Drug Discovery 7, no. 1 (January 1, 2013): 11–25. http://dx.doi.org/10.2174/187221413804660953.

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Srinivasan, Venkataramanujam, Yoshiji Ohta, Javier Espino, Jose A. Pariente, Ana B. Rodriguez, Mahaneem Mohamed, and Rahimah Zakaria. "Metabolic Syndrome, its Pathophysiology and the Role of Melatonin." Recent Patents on Endocrine, Metabolic & Immune Drug Discovery 7, no. 1 (December 1, 2012): 11–25. http://dx.doi.org/10.2174/1872214811307010011.

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Tosini, Gianluca, Kenkichi Baba, Christopher K. Hwang, and P. Michael Iuvone. "Melatonin: An underappreciated player in retinal physiology and pathophysiology." Experimental Eye Research 103 (October 2012): 82–89. http://dx.doi.org/10.1016/j.exer.2012.08.009.

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Ivanov, Dmitry O., Inna I. Evsyukova, Gianluigi Mazzoccoli, George Anderson, Victoria O. Polyakova, Igor M. Kvetnoy, Annalucia Carbone, and Ruslan A. Nasyrov. "The Role of Prenatal Melatonin in the Regulation of Childhood Obesity." Biology 9, no. 4 (April 5, 2020): 72. http://dx.doi.org/10.3390/biology9040072.

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There is a growing awareness that pregnancy can set the foundations for an array of diverse medical conditions in the offspring, including obesity. A wide assortment of factors, including genetic, epigenetic, lifestyle, and diet can influence foetal outcomes. This article reviews the role of melatonin in the prenatal modulation of offspring obesity. A growing number of studies show that many prenatal risk factors for poor foetal metabolic outcomes, including gestational diabetes and night-shift work, are associated with a decrease in pineal gland-derived melatonin and associated alterations in the circadian rhythm. An important aspect of circadian melatonin’s effects is mediated via the circadian gene, BMAL1, including in the regulation of mitochondrial metabolism and the mitochondrial melatoninergic pathway. Alterations in the regulation of mitochondrial metabolic shifts between glycolysis and oxidative phosphorylation in immune and glia cells seem crucial to a host of human medical conditions, including in the development of obesity and the association of obesity with the risk of other medical conditions. The gut microbiome is another important hub in the pathoetiology and pathophysiology of many medical conditions, with negative consequences mediated by a decrease in the short-chain fatty acid, butyrate. The effects of butyrate are partly mediated via an increase in the melatoninergic pathway, indicating interactions of the gut microbiome with melatonin. Some of the effects of melatonin seem mediated via the alpha 7 nicotinic receptor, whilst both melatonin and butyrate may regulate obesity through the opioidergic system. Oxytocin, a recently recognized inhibitor of obesity, may also be acting via the opioidergic system. The early developmental regulation of these processes and factors by melatonin are crucial to the development of obesity and many diverse comorbidities.

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Alawad, Zainab M., and Hanan L. Al-Omary. "Melatonin in male and female fertility." AL-Kindy College Medical Journal 17, no. 3 (December 30, 2021): 145–51. http://dx.doi.org/10.47723/kcmj.v17i3.398.

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Melatonin, a hormone synthesized mainly by the pineal gland, has been found in extra-pineal organs as well. It’s known as an organizer of circadian rhythms and more recently as an anti-oxidant. In addition to its role in maintaining immunity, pathophysiology of cardiovascular and neurological diseases, and as an anti-cancer agent, evidence has demonstrated that melatonin exerts a positive impact on male and female fertility primarily through oxygen scavenging effects. In In Vitro Fertilization (IVF) programs, supplementation of melatonin may be associated with better outcomes in terms of sperm quality, oocyte quality, embryo quality and pregnancy rates. This review summarizes various actions of melatonin on the body focusing on male and female fecundity.

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Tom, B., P. De Vries, JPC Heiligers, EW Willems, E. Scalbert, P. Delagrange, and PR Saxena. "The Lack of Vasoconstrictor Effect of the Pineal Hormone Melatonin in an Animal Model Predictive of Antimigraine Activity." Cephalalgia 21, no. 6 (July 2001): 656–63. http://dx.doi.org/10.1046/j.1468-2982.2001.00215.x.

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The pineal hormone, melatonin, has been implicated in the pathophysiology of migraine and several studies have demonstrated its vasoconstrictor properties. In the present study, systemic and carotid haemodynamic effects of melatonin, administered directly into the carotid artery, were investigated in anaesthetized pigs. Ten-minute intracarotid infusions of melatonin (1, 10 and 100 μg kg−1 min−1) produced slight decreases in blood pressure and total carotid and arteriovenous anastomotic blood flows, but nutrient blood flow was not affected. The decrease in carotid blood flow was entirely caused by the hypotension, since no changes in vascular conductance values were observed. It is concluded that melatonin itself is not capable of producing vasoconstriction in the cranial circulation of anaesthetized pigs. Thus, it appears that melatonin has no anti-migraine potential via a vasoconstrictor mechanism.

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Won, Eunsoo, Kyoung-Sae Na, and Yong-Ku Kim. "Associations between Melatonin, Neuroinflammation, and Brain Alterations in Depression." International Journal of Molecular Sciences 23, no. 1 (December 28, 2021): 305. http://dx.doi.org/10.3390/ijms23010305.

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Pro-inflammatory systemic conditions that can cause neuroinflammation and subsequent alterations in brain regions involved in emotional regulation have been suggested as an underlying mechanism for the pathophysiology of major depressive disorder (MDD). A prominent feature of MDD is disruption of circadian rhythms, of which melatonin is considered a key moderator, and alterations in the melatonin system have been implicated in MDD. Melatonin is involved in immune system regulation and has been shown to possess anti-inflammatory properties in inflammatory conditions, through both immunological and non-immunological actions. Melatonin has been suggested as a highly cytoprotective and neuroprotective substance and shown to stimulate all stages of neuroplasticity in animal models. The ability of melatonin to suppress inflammatory responses through immunological and non-immunological actions, thus influencing neuroinflammation and neurotoxicity, along with subsequent alterations in brain regions that are implicated in depression, can be demonstrated by the antidepressant-like effects of melatonin. Further studies that investigate the associations between melatonin, immune markers, and alterations in the brain structure and function in patients with depression could identify potential MDD biomarkers.

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Tortosa, Federico, Manuel Puig-Domingo, Miguel-Angel Peinado, Josep Oriola, Susan M. Webb, and Alberto de Leiva. "Enhanced circadian rhythm of melatonin in anorexia nervosa." Acta Endocrinologica 120, no. 5 (May 1989): 574–78. http://dx.doi.org/10.1530/acta.0.1200574.

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Abstract. Plasma melatonin circadian profiles were investigated in a group of 4 patients with anorexia nervosa and 4 healthy regularly cycling women. There were no differences in the mean age of both groups, whereas the anorexia nervosa patients had lower mean body weight (37.8 ± 2.0 vs 57.0 ± 4.9 kg) and body mass index (13.9 ± 1.1 vs 20.8 ± 2.0). Samples were collected every 2 h and plasma melatonin was measured by using a RIA with an iodinated tracer. Anorexia nervosa patients exhibited higher diurnal (60.7 ± 1.8 vs 25.4 ± 1.72 pmol/l, P< 0.02) and nocturnal (419.2 ± 37.4 vs 108.0 ± 33.6 pmol/l), P< 0.001) mean plasma melatonin concentrations. There were no differences in the time peak for nocturnal melatonin secretion in both groups, detected at 02.00 h. In anorexia nervosa, the melatonin circadian profile paralleled that observed in the control group, indicating that the increased melatonin values for anorexia nervosa were probably due to an enhanced secretory pineal function rather than an impaired melatonin metabolism. These results suggest a participation of the pineal gland in the pathophysiology of anorexia nervosa.

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Souza, Elisberto Nogueira de, Pedro Walisson Gomes Feitosa, Marcos Ryan Barbosa Rodrigues, Rian Brito Teles, Melina Maria Batista Silva, and Caroline De Almeida Cabral Ribeiro. "A Fisiofarmacologia da Melatonina no Desenvolvimento e Terapêutica do Câncer / The physiopharmacology of melatonin in cancer development and therapy." ID on line. Revista de psicologia 16, no. 60 (May 30, 2022): 754–77. http://dx.doi.org/10.14295/idonline.v16i60.3459.

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Resumo:Hodiernamente, umas das patologias com maior índice de mortalidade e morbidade prevalente em todo o mundo é o câncer, um dos maiores desafios da saúde pública no Brasil e no mundo. A melatonina é um hormônio natural regulador do sono produzido de forma endógena no organismo e secretado majoritariamente pela glândula pineal cujos efeitos possuem diversas relações intrínsecas no mecanismo fisiopatológico do desenvolvimento de neoplasias celulares. Este artigo trata-se de uma revisão bibliográfica realizada a partir da literatura médica online disponível na base de dados Public Medline (PUBMED) e pelo banco de dados da Biblioteca Virtual em Saúde (BVS), onde foram aplicados os descritores em saúde “Melatonin” e “Cancer”. No decorrer da pesquisa, foram abordados 3 temas principais: a fisiopatologia do câncer, a farmacologia da melatonina e as ações antineoplásicas desse hormônio no organismo. Resumidamente, agrupamos estas ações antitumorais em 5 grandes áreas: efeito antioxidante, efeito antiproliferativo, efeito imunomodulador, potencial como coadjuvante quimiorradioterápico e potencial como marcador biológico. Em síntese, portanto, nossa pesquisa busca evidenciar a importância da inserção desse hormônio natural em densas pesquisas científicas que devem ser realizadas com o intuito de beneficiar não somente os portadores de câncer como também a humanidade em geral.Palavras-chave: Câncer. Melatonina. Fisiofarmacologia. Tratamento. Abstract:Today, one of the pathologies with the highest mortality and morbidity rates prevalent worldwide is cancer, one of the greatest public health challenges in Brazil and worldwide. Melatonin is a natural sleep regulating hormone produced endogenously in the body and secreted mainly by the pineal gland. Common effects have several intrinsic relationships in the pathophysiological mechanism of the development of cell neoplasms. This article is a bibliographic review based on the online medical literature available in the Public Medline database (PUBMED) and in the database of the brazilian Virtual Health Library (VHL), where the health descriptors “Melatonin” and "Cancer" were applied. During the research, the three main themes were: the pathophysiology of cancer, the pharmacology of melatonin and the antineoplastic actions of this hormone in the body. Briefly, we have grouped these antitumor actions into 5 major areas: antioxidant effect, antiproliferative effect, immunomodulatory effect, potential as a chemoradiotherapeutic adjunct and potential as a biological marker. In summary, therefore, our research seeks to highlight the importance of inserting this natural hormone in dense scientific research that must be carried out in order to benefit not only cancer patients but also humanity in general.Keywords: Cancer. Melatonin. Physiopharmacology. Treatment.

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Li, Yiran, Sze-Wan Hung, Ruizhe Zhang, Gene Chi-Wai Man, Tao Zhang, Jacqueline Pui-Wah Chung, Lanlan Fang, and Chi-Chiu Wang. "Melatonin in Endometriosis: Mechanistic Understanding and Clinical Insight." Nutrients 14, no. 19 (October 1, 2022): 4087. http://dx.doi.org/10.3390/nu14194087.

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Endometriosis is defined as the development of endometrial glands and stroma outside the uterine cavity. Pathophysiology of this disease includes abnormal hormone profiles, cell survival, migration, invasion, angiogenesis, oxidative stress, immunology, and inflammation. Melatonin is a neuroendocrine hormone that is synthesized and released primarily at night from the mammalian pineal gland. Increasing evidence has revealed that melatonin can be synthesized and secreted from multiple extra-pineal tissues where it regulates immune response, inflammation, and angiogenesis locally. Melatonin receptors are expressed in the uterus, and the therapeutic effects of melatonin on endometriosis and other reproductive disorders have been reported. In this review, key information related to the metabolism of melatonin and its biological effects is summarized. Furthermore, the latest in vitro and in vivo findings are highlighted to evaluate the pleiotropic functions of melatonin, as well as to summarize its physiological and pathological effects and treatment potential in endometriosis. Moreover, the pharmacological and therapeutic benefits derived from the administration of exogenous melatonin on reproductive system-related disease are discussed to support the potential of melatonin supplements toward the development of endometriosis. More clinical trials are needed to confirm its therapeutic effects and safety.

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Bilski, Bartosz, Paweł Rzymski, Katarzyna Tomczyk, and Izabela Rzymska. "The impact of factors in work environment (especially shift and night work) on neoplasia of female reproductive organs." Journal of Medical Science 84, no. 4 (December 30, 2015): 223–28. http://dx.doi.org/10.20883/medical.e3.

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Shift work, due to disruption of circadian rhythms, can interfere with a number of physiological functions. It may lead to multiple pathologies (functional gastrointestinal disorders, peptic ulcer disease, hormonal disorders – including impaired melatonin secretion, cardiovascular disease, mental disabilities, neurological disorders etc.). In the last few years, we started to think about the association between disruption in melatonin secretion and the occurrence of certain malignancies. Authors describe and discuss pathophysiology, epidemiological and clinical data concerning influence of shift work to occurrence of some neoplasms.

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Dmitrzak-Weglarz, Monika, and Edyta Reszka. "Pathophysiology of Depression: Molecular Regulation of Melatonin Homeostasis – Current Status." Neuropsychobiology 76, no. 3 (2017): 117–29. http://dx.doi.org/10.1159/000489470.

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Tamtaji, Omid Reza, Moein Mobini, Amir Abbas Atlasi, Ehsan Dadgostar, and Zatollah Asemi. "Melatonin and oral squamous cell carcinoma: current knowledge and future perspectives." Melatonin Research 2, no. 1 (February 16, 2019): 94–105. http://dx.doi.org/10.32794/mr11250013.

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On the basis of worldwide ranking, oral cancer is the eighth most prevalent cancer. Oral squamous cell carcinoma is a cancer that occurs following dysplasia of the mucosa of the oral cavity and oropharynx. There are different inflammatory pathways involved in the pathophysiology of oral squamous cell carcinoma. Melatonin (N-acetyl-5-methoxytryptamine), a well documented anticancer agent, exhibits numerous functions including induction of apoptotic pathways and controlling of oxidative stress. In the in vivo and in vitro studies the results have demonstrated that melatonin supplementation is an appropriate therapeutic approach for oral squamous cell carcinoma. Melatonin might inhibit cancer cells through the regulation of molecular pathways including AKT/mTOR pathway, ERK/AKT signaling, LSD1 expression and tumor-associated neutrophils releasing. Limited clinical studies; however, have evaluated the role of melatonin in oral squamous cell carcinoma. This review summarizes current knowledge and evidence regarding the effects of melatonin on oral squamous cell carcinoma and the mechanisms involved.

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Campos, Luciana A., Jose Cipolla-Neto, Fernanda G. Amaral, Lisete C. Michelini, Michael Bader, and Ovidiu C. Baltatu. "The Angiotensin-Melatonin Axis." International Journal of Hypertension 2013 (2013): 1–7. http://dx.doi.org/10.1155/2013/521783.

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Accumulating evidence indicates that various biological and neuroendocrine circadian rhythms may be disrupted in cardiovascular and metabolic disorders. These circadian alterations may contribute to the progression of disease. Our studies direct to an important role of angiotensin II and melatonin in the modulation of circadian rhythms. The brain renin-angiotensin system (RAS) may modulate melatonin synthesis, a hormone with well-established roles in regulating circadian rhythms. Angiotensin production in the central nervous system may not only influence hypertension but also appears to affect the circadian rhythm of blood pressure. Drugs acting on RAS have been proven effective in the treatment of cardiovascular and metabolic disorders including hypertension and diabetes mellitus (DM). On the other hand, since melatonin is capable of ameliorating metabolic abnormalities in DM and insulin resistance, the beneficial effects of RAS blockade could be improved through combined RAS blocker and melatonin therapy. Contemporary research is evidencing the existence of specific clock genes forming central and peripheral clocks governing circadian rhythms. Further research on the interaction between these two neurohormones and the clock genes governing circadian clocks may progress our understanding on the pathophysiology of disease with possible impact on chronotherapeutic strategies.

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Anderson, George, Annalucia Carbone, and Gianluigi Mazzoccoli. "Tryptophan Metabolites and Aryl Hydrocarbon Receptor in Severe Acute Respiratory Syndrome, Coronavirus-2 (SARS-CoV-2) Pathophysiology." International Journal of Molecular Sciences 22, no. 4 (February 5, 2021): 1597. http://dx.doi.org/10.3390/ijms22041597.

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The metabolism of tryptophan is intimately associated with the differential regulation of diverse physiological processes, including in the regulation of responses to severe acute respiratory syndrome, coronavirus-2 (SARS-CoV-2) infection that underpins the COVID-19 pandemic. Two important products of tryptophan metabolism, viz kynurenine and interleukin (IL)4-inducible1 (IL41)-driven indole 3 pyruvate (I3P), activate the aryl hydrocarbon receptor (AhR), thereby altering the nature of immune responses to SARS-CoV-2 infection. AhR activation dysregulates the initial pro-inflammatory cytokines production driven by neutrophils, macrophages, and mast cells, whilst AhR activation suppresses the endogenous antiviral responses of natural killer cells and CD8+ T cells. Such immune responses become further dysregulated by the increased and prolonged pro-inflammatory cytokine suppression of pineal melatonin production coupled to increased gut dysbiosis and gut permeability. The suppression of pineal melatonin and gut microbiome-derived butyrate, coupled to an increase in circulating lipopolysaccharide (LPS) further dysregulates the immune response. The AhR mediates its effects via alterations in the regulation of mitochondrial function in immune cells. The increased risk of severe/fatal SARS-CoV-2 infection by high risk conditions, such as elderly age, obesity, and diabetes are mediated by these conditions having expression levels of melatonin, AhR, butyrate, and LPS that are closer to those driven by SARS-CoV-2 infection. This has a number of future research and treatment implications, including the utilization of melatonin and nutraceuticals that inhibit the AhR, including the polyphenols, epigallocatechin gallate (EGCG), and resveratrol.

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Anderson, George, and Gianluigi Mazzoccoli. "Left Ventricular Hypertrophy: Roles of Mitochondria CYP1B1 and Melatonergic Pathways in Co-Ordinating Wider Pathophysiology." International Journal of Molecular Sciences 20, no. 16 (August 20, 2019): 4068. http://dx.doi.org/10.3390/ijms20164068.

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Left ventricular hypertrophy (LVH) can be adaptive, as arising from exercise, or pathological, most commonly when driven by hypertension. The pathophysiology of LVH is consistently associated with an increase in cytochrome P450 (CYP)1B1 and mitogen-activated protein kinases (MAPKs) and a decrease in sirtuins and mitochondria functioning. Treatment is usually targeted to hypertension management, although it is widely accepted that treatment outcomes could be improved with cardiomyocyte hypertrophy targeted interventions. The current article reviews the wide, but disparate, bodies of data pertaining to LVH pathoetiology and pathophysiology, proposing a significant role for variations in the N-acetylserotonin (NAS)/melatonin ratio within mitochondria in driving the biological underpinnings of LVH. Heightened levels of mitochondria CYP1B1 drive the ‘backward’ conversion of melatonin to NAS, resulting in a loss of the co-operative interactions of melatonin and sirtuin-3 within mitochondria. NAS activates the brain-derived neurotrophic factor receptor, TrkB, leading to raised trophic signalling via cyclic adenosine 3′,5′-monophosphate (cAMP)-response element binding protein (CREB) and the MAPKs, which are significantly increased in LVH. The gut microbiome may be intimately linked to how stress and depression associate with LVH and hypertension, with gut microbiome derived butyrate, and other histone deacetylase inhibitors, significant modulators of the melatonergic pathways and LVH more generally. This provides a model of LVH that has significant treatment and research implications.

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Kedarisetty, Chandan Kumar, B. Laksminarayana Samaga, Sudha Vidyasagar, and Jayanthi Venkataraman. "Oral melatonin improves the detection of parasitemia in malaria." Journal of Infection in Developing Countries 14, no. 11 (November 30, 2020): 1327–31. http://dx.doi.org/10.3855/jidc.12518.

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Introduction: Malaria is a growing global threat and a major cause of mortality in the tropics. The gold standard diagnosis is peripheral blood smear examination. It has been demonstrated that melatonin acts as messenger molecule in malaria pathophysiology. This concept was used to evolve a clinical study wherein use of exogenous melatonin could improve the chance of detection of the parasite. Methodology: In a prospective study, 80 consecutive patients seen in the Department of Medicine at Kasturba Hospital, Manipal, suspected to have malarial fever were enrolled with proper informed consent, and randomly assigned to the groups given oral melatonin 3mg (melatonin group, n = 40) or placebo (control group, n = 40). Blood samples were collected for peripheral smear examination at baseline and then at two, three, four and five hours after drug administration. The primary end point was the parasite detection index. Results: Baseline characteristics of patients were comparable. In the melatonin group, there was a significant increase of 0.0943 ± 0.22 in the mean parasite index from 0.217 ± 0.42 pre-melatonin to 0.3114 ± 0.5 post-melatonin (p = 0.001), compared to a difference of 0.0025 ± 0.22 in mean parasite index before and after placebo in the control group (p = 0.95). The maximum rise in parasite detection was seen at five hours after melatonin. Conclusions: In a single centre study, for the first time, it has been shown that a significantly higher proportion of patients was diagnosed with malaria on peripheral smear after oral melatonin administration, maximal at five hours after administration of melatonin.

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Huang, Yue-bo, Ling Jiang, Xue-qi Liu, Xian Wang, Li Gao, Han-xu Zeng, Wei Zhu, Xue-ru Hu, and Yong-gui Wu. "Melatonin Alleviates Acute Kidney Injury by Inhibiting NRF2/Slc7a11 Axis-Mediated Ferroptosis." Oxidative Medicine and Cellular Longevity 2022 (August 8, 2022): 1–24. http://dx.doi.org/10.1155/2022/4776243.

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Acute kidney injury (AKI) is still a puzzling clinical problem; its pathophysiology is not completely understood. Up to now, an effective treatment for AKI is lacking. Ferroptosis is a novel form of regulated cell death characterized by the lethal accumulation of lipid hydroperoxides that are dependent on iron and reactive oxygen species and mitochondrial dysfunction. Recently, ferroptosis was shown to play a vital role in AKI such as ischemia-reperfusion kidney injury and folic acid-induced AKI. Melatonin (MT) is an antioxidant that regulates the sleep-wake cycle. While the therapeutic effect of melatonin on AKI has been reported, its mechanism for the treatment of renal ferroptosis remains unclear. We found that melatonin treatment significantly alleviated the serum biochemistry index and histopathological alterations in vivo AKI models induced by bilateral renal artery ischemia reperfusion and folic acid in mice. Ferroptosis induced by hypoxia and reoxygenation or erastin (Era) in mouse tubular epithelial cells (MTEC) was also rescued by melatonin treatment. RNA sequence analysis of ferroptosis-related genes showed that melatonin affects oxidative stress responses by inhibiting hypoxia and reoxygenation- (HR-) mediated downregulation of NRF2 and upregulation of Slc7a11 in MTEC. Specific knockdown of NRF2 increased the sensitivity of cells to ferroptosis, and melatonin failed to protect against ferroptosis in the HR condition. Together, our data indicate that melatonin prevents ferroptosis in AKI by acting on the NRF2/Slc7a11 axis.

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Anderson, George. "Daytime orexin and night-time melatonin regulation of mitochondria melatonin: roles in circadian oscillations systemically and centrally in breast cancer symptomatology." Melatonin Research 2, no. 4 (December 15, 2019): 1–8. http://dx.doi.org/10.32794/mr11250037.

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This article reviews the recent proposed model of Reiter and colleagues in this journal on the role of circadian, pineal gland-derived melatonin in driving mitochondria melatonin production in the pathoetiology and pathophysiology of breast cancers. This uptake of melatonin is proposed to inhibit pyruvate dehydrogenase kinase, thereby increasing the production of acetyl-CoA from pyruvate, with acetyl-CoA being a necessary co-factor for the initiation of the melatonergic pathway within mitochondria. Consequently, this proposed model suggests that a circadian shift in metabolic regulation occurs in breast cancers, from daytime cytosolic glycolysis to a night-time, melatonin-driven mitochondria oxidative phosphorylation, with relevance to the early pathoetiology of breast cancers. This has a number of consequences and links well to wider breast cancer data showing a pathophysiological role for the aryl hydrocarbon receptor, cytochrome P450 (CYP)1B1, 14-3-3 protein, and microRNAs. The current article overviews such data in the context of pineal gland-derived melatonin's circadian regulation of the mitochondria melatonergic pathways in breast cancer cells as proposed by Reiter and colleagues, suggesting that daytime, wake promoting orexin and stress-induced gut dysregulation contribute to mitochondria dysfunction in wider breast cancer symptomatology.

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Anderson, George. "Mitochondria and the Gut as crucial hubs for the interactions of melatonin with sirtuins, inflammation, butyrate, tryptophan metabolites, and alpha 7 nicotinic receptor across a host of medical conditions." Melatonin Research 2, no. 2 (June 12, 2019): 70–85. http://dx.doi.org/10.32794/mr11250022.

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Two important hubs have emerged as cutting edge areas of research across a diverse array of medical conditions, the gut microbiome and mitochondria. This article highlights the role of melatonin in modulating changes in both the gut and mitochondria. The gut microbiome, especially via its production of the small chain fatty acid, butyate, can have a significant impact on immune inflammatory processes. Lower levels of butyrate producing bacteria can increase gut permeability, thereby increasing immune-inflammatory activity. Butyrate may also modulate immune and other cells via the regulation of the content of exosomes from intestinal epithelial cells. Butyrate also induces N-acetylserotonin and melatonin synthesis in the gut, suggesting that some of the effects of butyrate may be mediated via its induction of the melatonergic pathway. The induction of melatonin by butyrate may feed back on the microbiome via melatonin increasing gut bacteria swarming, as well as melatonin optimizing gut barrier and mitochondria functioning. As butyrate readily crosses into the circulation it is likely that the immune- and glia-dampening effects of butyrate also involve the induction of melatonin in these reactive cells. Butyrate also positively modulates mitochondria functioning, suggesting that butyrate, both directly and via melatonin, will have significant impacts on gut, immune, glia and other cells, via mitochondria regulation. Other factors that act to regulate melatonin, including dietary factors and stress, will therefore act to modulate many of butyrate's effects. The regulation of melatonin at these two important hubs has significant treatment and classification implications across a wide array of medical conditions. Overall, gut dysbiosis has a significant impact on central and systemic homeostasis, via decreased butyrate and melatonin driving suboptimal mitochondria functioning. This has implications for the pathoetiology and pathophysiology of a host of medical conditions associated with gut dysbiosis and decreased melatonin production.

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Cosme, Patricia, Ana B. Rodríguez, María Garrido, and Javier Espino. "Coping with Oxidative Stress in Reproductive Pathophysiology and Assisted Reproduction: Melatonin as an Emerging Therapeutical Tool." Antioxidants 12, no. 1 (December 30, 2022): 86. http://dx.doi.org/10.3390/antiox12010086.

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Infertility is an increasing global public health concern with socio-psychological implications for affected couples. Remarkable advances in reproductive medicine have led to successful treatments such as assisted reproductive techniques (ART). However, the search for new therapeutic tools to improve ART success rates has become a research hotspot. In the last few years, pineal indolamine melatonin has been investigated for its powerful antioxidant properties and its role in reproductive physiology. It is considered a promising therapeutical agent to counteract the detrimental effects associated with oxidative stress in fertility treatments. The aim of the present narrative review was to summarize the current state of the art on the importance of melatonin in reproductive physiology and to provide a critical evaluation of the data available encompassing basic, translational and clinical studies on its potential use in ART to improve fertility success rates.

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Satyanarayanan, Senthil Kumaran, Huanxing Su, Yi-Wen Lin, and Kuan-Pin Su. "Circadian Rhythm and Melatonin in the Treatment of Depression." Current Pharmaceutical Design 24, no. 22 (October 19, 2018): 2549–55. http://dx.doi.org/10.2174/1381612824666180803112304.

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Background: Circadian rhythm disruption underlies the pathophysiology of psychiatric disorders, especially depression. Both pharmacological and non-pharmacological strategies affecting endogenous circadian rhythms have been developed with specificity to alter the circadian dysfunction. The current management strategy with antidepressants is far from being satisfactory in addressing this issue. In recent years, attempts at discovering new antidepressants focused on a melatonergic system which is known to be altered in depression have led to a potential option for treatment of depression. Methods: We reviewed all recently published relevant articles on melatonin and its analogues to look for their implication in the treatment of circadian rhythm disruption and depression. Results: Melatonin, a pleiotropic regulator molecule and its analogues (ramelteon, agomelatine, TIK-301, Neu- P11 and tasimelteon) have been observed to resynchronize the circadian rhythm and some were said to alleviate depressive symptoms in depressed subjects. Conclusion: This review focuses on substantial advances in the melatonin-based chronobiologic intervention and its responses in the treatment of depression.

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Varga, Noemi, Juan Carlos Ruiz-Rodríguez, and Ricard Ferrer. "Melatonin and mitochondrial dysfunction are key players in the pathophysiology of sepsis." Enfermedades Infecciosas y Microbiología Clínica 36, no. 9 (November 2018): 535–38. http://dx.doi.org/10.1016/j.eimc.2018.07.001.

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Varga, Noemi, Juan Carlos Ruiz-Rodríguez, and Ricard Ferrer. "Melatonin and mitochondrial dysfunction are key players in the pathophysiology of sepsis." Enfermedades infecciosas y microbiologia clinica (English ed.) 36, no. 9 (November 2018): 535–38. http://dx.doi.org/10.1016/j.eimce.2018.07.012.

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Anderson, George, and Russel J. Reiter. "COVID-19 pathophysiology: interactions of gut microbiome, melatonin, vitamin D, stress, kynurenine and the alpha 7 nicotinic receptor: Treatment implications." Melatonin Research 3, no. 3 (June 15, 2020): 322–45. http://dx.doi.org/10.32794/mr11250066.

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As data emerges on the pathophysiological underpinnings of severe acute respiratory syndrome coronavirus (SARS-CoV)-2, it is clear that there are considerable variations in its susceptibility and severity/fatality, which give indications as to its pathophysiology and treatment. SARS-CoV-2 modulatory factors include age, vitamin D levels, cigarette smoking, gender and ethnicity as well as premorbid medical conditions, including diabetes, cancer, obesity, cardiovascular disease, and immune-compromised conditions. A complex picture is emerging, with an array of systemic physiological processes interacting including circadian, immune, intestinal, CNS and coagulation factors. This article reviews data on SARS-CoV-2 pathoetiology and pathophysiology. It is proposed that a decrease in pineal and systemic melatonin is an important driver of SARS-CoV-2 susceptibility and severity, with the loss of pineal melatonin's induction of the alpha 7 nicotinic acetylcholine receptor (α7nAChR) in pulmonary epithelial cells and immune cells being a powerful regulator of susceptibility and severity, respectively. Stress, including discrimination stress, and decreased vitamin D also regulate SARS-CoV-2, including via gut dysbiosis and permeability, with a resultant decrease in the short-chain fatty acid, butyrate, and increase in circulating lipopolysaccharide. Stress and cytokine induction of the kynurenine pathways, leads to aryl hydrocarbon receptor activation, which primes platelets for heightened activity, coagulation and thrombin production, thereby driving elevations in thrombin that underpin many SARS-CoV-2 fatalities. On the basis of these pathophysiological changes, prophylactic and symptomatic treatments are proposed, including the use of melatonin and α7nAChR agonism.

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Vidiker, R. V., N. V. Trubina, and A. R. Babaeva. "Circulating neurotransmitter levels in irritable bowel syndrome: correlation of laboratory tests and clinical findings." South Russian Journal of Therapeutic Practice 1, no. 2 (September 15, 2020): 72–77. http://dx.doi.org/10.21886/2712-8156-2020-1-2-72-77.

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Objective: to estimate blood levels of serotonin and melatonin neurotransmitters in patients with irritable bowel syndrome and to evaluate the role of neurohumoral imbalance in the development and clinical manifestations of irritable bowel syndrome phenotypes.Materials and methods: the study included 60 patients (range, 18 – 45 years) diagnosed with irritable bowel syndrome according to the Roman IV criteria for irritable bowel syndrome (2016). 20 patients with a confirmed diagnosis of ulcerative colitis (UC) were assigned to a comparison group. The control group was composed of 45 apparently healthy subjects. All subjects were assigned to subgroups based on the prominent clinical presentation: irritable bowel syndrome with constipation (IBS-C), irritable bowel syndrome with diarrhea (IBS-D) and mixed irritable bowel syndrome (IBS-M). In addition to all the necessary procedures (clinical, laboratory and instrumental), blood concentrations of endogenous serotonin and melatonin were measured using enzyme-linked immunosorbent assay (ELISA).Results: the concentrations of endogenous serotonin and melatonin were significantly lower in patients with irritable bowel syndrome as compared with those having ulcerative colitis or healthy individuals. The detection rates of lowering serotonin levels were 53.3 % and 65 % — for melatonin. Low levels of melatonin were detected both in IBS-D and IBS-C patients. 69.57 % of IBS-D patients had elevated levels of serotonin as compared with the reference values for healthy subjects. We found a strong correlation between the severity of bloating and abdominal pain on the one hand, and low levels of endogenous serotonin and melatonin, on the other hand.Conclusion: our findings suggest that serotonin and melatonin neurotransmitters play a significant role in the pathophysiology and clinical manifestations of estimate blood levels of serotonin and melatonin neurotransmitters in patients with irritable bowel syndrome.

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Maxwell, Marius, Dimitris Karacostas, Richard G. Ellenbogen, Amnon Brzezinski, Nicholas T. Zervas, and Peter McL Black. "Precocious puberty following head injury." Journal of Neurosurgery 73, no. 1 (July 1990): 123–29. http://dx.doi.org/10.3171/jns.1990.73.1.0123.

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✓ A 6-year-old girl developed secondary sexual characteristics 5 months after severe closed head injury. Endocrinological tests confirmed a pubertal sexual condition; there was also diminution of serum melatonin and disruption of the diurnal pattern. Magnetic resonance imaging demonstrated focal hypothalamic injury; this is believed to be the first time such a posttraumatic lesion has been demonstrated by imaging techniques. The pathophysiology of this condition is discussed.

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Bartakovicova, Kristina, Petra Kemenyova, Ivan Belica, Zofia Janik Szapuova, Katarina Stebelova, Iveta Waczulikova, Daniela Ostatnikova, and Katarina Babinska. "Sleep Problems and 6-Sulfatoxymelatonin as Possible Predictors of Symptom Severity, Adaptive and Maladaptive Behavior in Children with Autism Spectrum Disorder." International Journal of Environmental Research and Public Health 19, no. 13 (June 21, 2022): 7594. http://dx.doi.org/10.3390/ijerph19137594.

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In children with autism spectrum disorder (ASD), sleep disturbances are a frequent comorbidity with an adverse effect on their behavior and functioning. It was suggested that melatonin deficit is at least partly responsible for the sleep problems. The study aimed to investigate, in a sample of 56 children with ASD aged 2.8–13.3 years, if the sleep problems and melatonin secretion can serve as predictors of adaptive functioning and severity of the ASD core symptoms. We demonstrated that, after adjustment for age, the Sleep score assessed by the Children’s Sleep Habits Questionnaire predicts the Adaptive behavior composite score only in children younger than 6 years, and the preferred predictive model is for the domain Socialization. The age-adjusted Sleep score predicted Externalizing and Internalizing maladaptive behavior, with a near-zero contribution of age to the relationship between the Internalizing maladaptive behavior and Sleep score. After adjustment for age, the reduced night-time melatonin secretion predicted a higher severity of ASD symptoms in the domain Social affect and the Calibrated Severity Score, but not the sleep problems. Our results emphasize the importance of assessing sleep problems as a modifiable predictor of behavior in children with ASD and support the hypothesis about the role of melatonin in pathophysiology of ASD.

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Mota-Rojas, Daniel, Dina Villanueva-García, Alfonso Solimano, Ramon Muns, Daniel Ibarra-Ríos, and Andrea Mota-Reyes. "Pathophysiology of Perinatal Asphyxia in Humans and Animal Models." Biomedicines 10, no. 2 (February 1, 2022): 347. http://dx.doi.org/10.3390/biomedicines10020347.

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Perinatal asphyxia is caused by lack of oxygen delivery (hypoxia) to end organs due to an hypoxemic or ischemic insult occurring in temporal proximity to labor (peripartum) or delivery (intrapartum). Hypoxic–ischemic encephalopathy is the clinical manifestation of hypoxic injury to the brain and is usually graded as mild, moderate, or severe. The search for useful biomarkers to precisely predict the severity of lesions in perinatal asphyxia and hypoxic–ischemic encephalopathy (HIE) is a field of increasing interest. As pathophysiology is not fully comprehended, the gold standard for treatment remains an active area of research. Hypothermia has proven to be an effective neuroprotective strategy and has been implemented in clinical routine. Current studies are exploring various add-on therapies, including erythropoietin, xenon, topiramate, melatonin, and stem cells. This review aims to perform an updated integration of the pathophysiological processes after perinatal asphyxia in humans and animal models to allow us to answer some questions and provide an interim update on progress in this field.

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Johal, Arminder, Shalini Manchanda, Cynthia Bodkin, and Stephanie Stahl. "0813 Post-Pinealectomy Insomnia and Melatonin Therapy." Sleep 45, Supplement_1 (May 25, 2022): A352. http://dx.doi.org/10.1093/sleep/zsac079.809.

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Abstract Introduction Melatonin is a hormone produced in the pineal gland that has an important role in sleep; immune, neurologic, psychiatric, metabolic, and endocrinologic function; cardiac-autonomic regulation and even cancer risk. We present a case of insomnia, somnambulism, dream enactment, and periodic limb movements of sleep (PLMS) after a pinealectomy. Report of Cases: A 40-year-old woman with a history of a complete pinealectomy due to a pineal cyst presented to the sleep medicine clinic. Shortly after the pinealectomy, she developed sleep onset and maintenance insomnia. Two years later she developed somnambulism, and four years later she developed dream enactment and PLMS. She reported no prior treatments for her sleep issues, including no history of melatonin use. On average, her total sleep time (TST) was 2-8 hours/night with awakenings every 2 hours. Sleep latency was 10-45 minutes. Polysomnograghy demonstrated an apnea-hypopnea index of 0.6/hr, PLM index of 68.1/hr, normal REM atonia, and no complex behaviors. The patient started 1mg immediate release (IR) melatonin, which did not help her insomnia, but parasomnias resolved. She had improvement in her PLMS with iron supplementation and melatonin. The melatonin dose was increased to 3mg IR which helped increase her TST to 4-8 hours. She was switched to 3mg extended release (ER) melatonin, and then increased to 4mg ER. She obtained the most benefit for her insomnia with 1mg IR plus 4mg ER with sleep latency reduced to 5-10 minutes and TST improved up to 7.5 hours with rare awakenings. Conclusion Pinealectomy in humans is rarely reported. Most data about the consequences of pinealectomy and pathophysiology of melatonin come from animal research. Melatonin level after pinealectomy is often undetectable or severely diminished. Current limited literature on patients with pinealectomy consists of case reports about patients who experienced insomnia, non-24-hour sleep-wake rhythm disorder [SSM1] and mood disorders. Melatonin doses ranging from 0.5mg to 14mg IR and up to 5mg ER have been trialed with most patients having symptomatic improvement with doses above 3mg. We found that a combination of 1mg immediate and 4mg extended release melatonin was the most beneficial for our patient. Support (If Any)

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Brzezinski, Amnon, Seema Rai, Adyasha Purohit, and Seithikurippu R. Pandi-Perumal. "Melatonin, Clock Genes, and Mammalian Reproduction: What Is the Link?" International Journal of Molecular Sciences 22, no. 24 (December 8, 2021): 13240. http://dx.doi.org/10.3390/ijms222413240.

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Physiological processes and behaviors in many mammals are rhythmic. Recently there has been increasing interest in the role of circadian rhythmicity in the control of reproductive function. The circadian rhythm of the pineal hormone melatonin plays a role in synchronizing the reproductive responses of animals to environmental light conditions. There is some evidence that melatonin may have a role in the biological regulation of circadian rhythms and reproduction in humans. Moreover, circadian rhythms and clock genes appear to be involved in optimal reproductive performance. These rhythms are controlled by an endogenous molecular clock within the suprachiasmatic nucleus (SCN) in the hypothalamus, which is entrained by the light/dark cycle. The SCN synchronizes multiple subsidiary oscillators (clock genes) existing in various tissues throughout the body. The basis for maintaining the circadian rhythm is a molecular clock consisting of transcriptional/translational feedback loops. Circadian rhythms and clock genes appear to be involved in optimal reproductive performance. This mini review summarizes the current knowledge regarding the interrelationships between melatonin and the endogenous molecular clocks and their involvement in reproductive physiology (e.g., ovulation) and pathophysiology (e.g., polycystic ovarian syndrome).

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Srinivasan, Venkatramanujam, Charanjit Kaur, Seithikurippu Pandi-Perumal, Gregory M. Brown, and Daniel P. Cardinali. "Melatonin and Its Agonist Ramelteon in Alzheimer's Disease: Possible Therapeutic Value." International Journal of Alzheimer's Disease 2011 (2011): 1–15. http://dx.doi.org/10.4061/2011/741974.

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Alzheimer's disease (AD) is an age-associated neurodegenerative disease characterized by the progressive loss of cognitive function, loss of memory and insomnia, and abnormal behavioral signs and symptoms. Among the various theories that have been put forth to explain the pathophysiology of AD, the oxidative stress induced by amyloid β-protein (Aβ) deposition has received great attention. Studies undertaken on postmortem brain samples of AD patients have consistently shown extensive lipid, protein, and DNA oxidation. Presence of abnormal tau protein, mitochondrial dysfunction, and protein hyperphosphorylation all have been demonstrated in neural tissues of AD patients. Moreover, AD patients exhibit severe sleep/wake disturbances and insomnia and these are associated with more rapid cognitive decline and memory impairment. On this basis, the successful management of AD patients requires an ideal drug that besides antagonizing Aβ-induced neurotoxicity could also correct the disturbed sleep-wake rhythm and improve sleep quality. Melatonin is an effective chronobiotic agent and has significant neuroprotective properties preventing Aβ-induced neurotoxic effects in a number of animal experimental models. Since melatonin levels in AD patients are greatly reduced, melatonin replacement has the potential value to be used as a therapeutic agent for treating AD, particularly at the early phases of the disease and especially in those in whom the relevant melatonin receptors are intact. As sleep deprivation has been shown to produce oxidative damage, impaired mitochondrial function, neurodegenerative inflammation, and altered proteosomal processing with abnormal activation of enzymes, treatment of sleep disturbances may be a priority for arresting the progression of AD. In this context the newly introduced melatonin agonist ramelteon can be of much therapeutic value because of its highly selective action on melatonin MT1/MT2receptors in promoting sleep.

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Journal articles on the topic 'Melatonin – Pathophysiology'

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