Tae-Kang Kim, Adrian Fabisiak, Pawel Brzeminski, Russel J Reiter, Andrzej T Slominski
We are commenting recent discoveries on the presence of L-DOPA, dopamine, 5-hydroxytryptophan, tryptamine, serotonin, N-acetylserotonin, melatonin, 2-hydroxymelatonin, AFMK and AMK in honey. Serotonin and melatonin, products of the tryptophan metabolism, are widely produced in nature, serving as hormones, neurotransmitters, biological regulators, neurotransmitters and antioxidants, in a context dependent fashion. Dopamine and tryptamine are important neurotransmitters across different species. Honey is used as one of the most popular healthy food substances. Detection of above molecules in honey accompanied by detection of vitamin D3 and its hydroxyderivatives, is consistent with their detection in insects and plants. Their presence in honey enhances spectrum of its beneficial effects for human health and implicates that these molecules must play important role in social insects physiology, bees development and colony functions.
{"title":"Serotonin, melatonin and their precursors and metabolites and vitamin D<sub>3</sub> derivatives in honey.","authors":"Tae-Kang Kim, Adrian Fabisiak, Pawel Brzeminski, Russel J Reiter, Andrzej T Slominski","doi":"10.32794/mr112500137","DOIUrl":"https://doi.org/10.32794/mr112500137","url":null,"abstract":"<p><p>We are commenting recent discoveries on the presence of L-DOPA, dopamine, 5-hydroxytryptophan, tryptamine, serotonin, <i>N</i>-acetylserotonin, melatonin, 2-hydroxymelatonin, AFMK and AMK in honey. Serotonin and melatonin, products of the tryptophan metabolism, are widely produced in nature, serving as hormones, neurotransmitters, biological regulators, neurotransmitters and antioxidants, in a context dependent fashion. Dopamine and tryptamine are important neurotransmitters across different species. Honey is used as one of the most popular healthy food substances. Detection of above molecules in honey accompanied by detection of vitamin D<sub>3</sub> and its hydroxyderivatives, is consistent with their detection in insects and plants. Their presence in honey enhances spectrum of its beneficial effects for human health and implicates that these molecules must play important role in social insects physiology, bees development and colony functions.</p>","PeriodicalId":18604,"journal":{"name":"Melatonin Research","volume":"5 3","pages":"374-380"},"PeriodicalIF":0.0,"publicationDate":"2022-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10062416/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9275402","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Currently, cardiovascular diseases are still the number one killer in the world. These include hypertension, coronary heart disease, ischemic heart disease, myocardial infarction, congestive heart failure, cardiac arrhythmias, etc. One of the risk factors for cardiovascular diseases is environmental heavy metal pollution which makes the victims more vulnerable to sudden cardiac death. Chromium (Cr) is one of the metals. Cr(VI) is the most hazardous one among its variants. It is readily across the plasma membrane to cause oxidative damage to intracellular molecules including LDL, proteins, and DNA; therefore, promotes endothelial dysfunction and Ca2+ overload in the heart. As to its molecular mechanism, Cr(VI) downregulates the expressions of SIRTUINS, FOXOs, PGC-1α, and AMPK and upregulates the P53, Akt, and NF-κβ, causing alteration in metabolic pathways, inhibiting mitochondrial biogenesis, inducing autophagy and apoptosis. In addition, Cr(VI) alters the expressions of Th1 cytokines (IL-1β, IL-2, IL-12, TNF-α, and IFN-γ) as well as Th2 cytokines (IL-4, IL-5, and IL-10) to induce myocardial inflammation. Melatonin, a potent antioxidant, and an efficient metal chelator can neutralize almost all the alterations caused by Cr(VI). Thus, melatonin can be a selected molecule to protect against Cr(VI)-induced cardiovascular toxicity. This review highlights the etiology of Cr(VI) associated heart diseases and the potentiality of melatonin to prevent Cr(VI)-mediated cardiac oxidative stress, apoptosis and inflammation.
{"title":"The pleiotropic role of melatonin against chromium-induced cardiovascular infirmities: a mechanistic insight","authors":"P. Ghosh, T. Dey, D. Bandyopadhyay","doi":"10.32794/mr112500130","DOIUrl":"https://doi.org/10.32794/mr112500130","url":null,"abstract":"Currently, cardiovascular diseases are still the number one killer in the world. These include hypertension, coronary heart disease, ischemic heart disease, myocardial infarction, congestive heart failure, cardiac arrhythmias, etc. One of the risk factors for cardiovascular diseases is environmental heavy metal pollution which makes the victims more vulnerable to sudden cardiac death. Chromium (Cr) is one of the metals. Cr(VI) is the most hazardous one among its variants. It is readily across the plasma membrane to cause oxidative damage to intracellular molecules including LDL, proteins, and DNA; therefore, promotes endothelial dysfunction and Ca2+ overload in the heart. As to its molecular mechanism, Cr(VI) downregulates the expressions of SIRTUINS, FOXOs, PGC-1α, and AMPK and upregulates the P53, Akt, and NF-κβ, causing alteration in metabolic pathways, inhibiting mitochondrial biogenesis, inducing autophagy and apoptosis. In addition, Cr(VI) alters the expressions of Th1 cytokines (IL-1β, IL-2, IL-12, TNF-α, and IFN-γ) as well as Th2 cytokines (IL-4, IL-5, and IL-10) to induce myocardial inflammation. Melatonin, a potent antioxidant, and an efficient metal chelator can neutralize almost all the alterations caused by Cr(VI). Thus, melatonin can be a selected molecule to protect against Cr(VI)-induced cardiovascular toxicity. This review highlights the etiology of Cr(VI) associated heart diseases and the potentiality of melatonin to prevent Cr(VI)-mediated cardiac oxidative stress, apoptosis and inflammation.","PeriodicalId":18604,"journal":{"name":"Melatonin Research","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83029357","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
M. R. Peres, V. R. Miranda, A. D. de Souza, N. Morgon, V. Ximenes
N1-acetyl-N2-formyl-5-methoxykynuramine (AFMK) is one of the primary oxidation products of melatonin. There is growing evidence of its beneficial biological properties, including antioxidant features and modulators of cytokines and enzymes involved in the inflammatory process. Here, the autoxidation of melatonin mediated by UVC was studied regarding the formation of AFMK and the reaction mechanism. The parameters evaluated were irradiation, pH, dissolved oxygen, superoxide radical anion, and hydroxyl radical. We found that the AFMK yield is directly correlated with UVC irradiation. The AFMK concentration decreased 95% when a 280 nm cutoff filter blocked the irradiation. By removing the dissolved oxygen from the medium, the decrease was 90%. Superoxide dismutase, acting as a scavenger of superoxide radical anion, caused a 64% reduction. At pH 7.0, the AFMK yield was just 14% of those obtained at pH 10. These findings are consistent with a typical autoxidation reaction. In addition, the low yield of AFMK in the absence of UVC irradiation suggested that electronically excited melatonin is the species involved in the initial electron transfer. Density Functional Theory (DFT) calculations were performed to strengthen the proposal. Corroborant with the experimental results, the theoretical analyses revealed that electron transfer from melatonin to molecular oxygen is only energetically feasible in the excited state. In conclusion, the direct autoxidation of melatonin at excited state in alkaline pH is a straightforward approach to producing AFMK.
{"title":"Autoxidation of melatonin at excited state: mechanism proposal for formation of N1-acetyl-N2-formyl-5-methoxykynuramine","authors":"M. R. Peres, V. R. Miranda, A. D. de Souza, N. Morgon, V. Ximenes","doi":"10.32794/mr112500135","DOIUrl":"https://doi.org/10.32794/mr112500135","url":null,"abstract":"N1-acetyl-N2-formyl-5-methoxykynuramine (AFMK) is one of the primary oxidation products of melatonin. There is growing evidence of its beneficial biological properties, including antioxidant features and modulators of cytokines and enzymes involved in the inflammatory process. Here, the autoxidation of melatonin mediated by UVC was studied regarding the formation of AFMK and the reaction mechanism. The parameters evaluated were irradiation, pH, dissolved oxygen, superoxide radical anion, and hydroxyl radical. We found that the AFMK yield is directly correlated with UVC irradiation. The AFMK concentration decreased 95% when a 280 nm cutoff filter blocked the irradiation. By removing the dissolved oxygen from the medium, the decrease was 90%. Superoxide dismutase, acting as a scavenger of superoxide radical anion, caused a 64% reduction. At pH 7.0, the AFMK yield was just 14% of those obtained at pH 10. These findings are consistent with a typical autoxidation reaction. In addition, the low yield of AFMK in the absence of UVC irradiation suggested that electronically excited melatonin is the species involved in the initial electron transfer. Density Functional Theory (DFT) calculations were performed to strengthen the proposal. Corroborant with the experimental results, the theoretical analyses revealed that electron transfer from melatonin to molecular oxygen is only energetically feasible in the excited state. In conclusion, the direct autoxidation of melatonin at excited state in alkaline pH is a straightforward approach to producing AFMK.","PeriodicalId":18604,"journal":{"name":"Melatonin Research","volume":"27 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81027804","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Melatonin and its metabolites are ubiquitous antioxidants that are produced in response to reactive oxygen species (ROS) in virtually all cells of the body. The highest reported melatonin values in plasma and sweat occur during heavy exercise both indoors and outdoors during the day. The advent of sweat biosensors with sufficient melatonin sensitivity provides pseudo real-time evidence that melatonin is produced throughout the body not just in the pineal gland. The role of the pineal gland appears to be to provide cyclic production of melatonin for the regulation of circadian rhythms as well as supplemental melatonin during periods of low cellular activity. Melatonin from the pineal gland represents only a small fraction of the body’s production capacity. Greater than 5 pg/ml min ramp rates for plasma and sweat melatonin have been reported during strenuous exercise in sunlight as compared to 0.15 pg/ml min ramp rates for plasma melatonin under dim light melatonin onset (DLMO) conditions. Sunlight and exercise, like fever, generates transient elevated levels of ROS in tissues with time constants measured in minutes or even seconds making this systemic antioxidant response potentially protective. Based on a simple accounting of ROS generated by sunlight, ROS we breathe, ROS we drink, and exercise, it appears that the body maintains a heightened basal level of ROS as part of its pathogen defense mechanisms. Current human lifestyles and modern enclosed spaces have substantially eliminated over 90% of the ROS which undermines one of the body’s primary defenses. With advanced age, the inability to maintain this protective barrier appears to make us more susceptible to disease.
{"title":"Transient responses of melatonin to stress","authors":"S. Zimmerman, R. Reiter","doi":"10.32794/mr112500133","DOIUrl":"https://doi.org/10.32794/mr112500133","url":null,"abstract":"Melatonin and its metabolites are ubiquitous antioxidants that are produced \u0000in response to reactive oxygen species (ROS) in virtually all cells of the \u0000body. The highest reported melatonin values in plasma and sweat occur during \u0000heavy exercise both indoors and outdoors during the day. The advent of sweat \u0000biosensors with sufficient melatonin sensitivity provides pseudo real-time \u0000evidence that melatonin is produced throughout the body not just in the pineal \u0000gland. The role of the pineal gland appears to be to provide cyclic production \u0000of melatonin for the regulation of circadian rhythms as well as supplemental melatonin \u0000during periods of low cellular activity. \u0000Melatonin from the pineal gland represents only a small fraction of the \u0000body’s production capacity. Greater than 5 pg/ml min ramp rates for plasma and \u0000sweat melatonin have been reported during strenuous exercise in sunlight as \u0000compared to 0.15 pg/ml min ramp rates for plasma melatonin under dim light \u0000melatonin onset (DLMO) conditions. Sunlight \u0000and exercise, like fever, generates transient elevated levels of ROS in tissues \u0000with time constants measured in minutes or even seconds making this systemic \u0000antioxidant response potentially protective. Based on a simple accounting of \u0000ROS generated by sunlight, ROS we breathe, ROS we drink, and exercise, it \u0000appears that the body maintains a heightened basal level of ROS as part of its \u0000pathogen defense mechanisms. Current \u0000human lifestyles and modern enclosed spaces have substantially eliminated over \u000090% of the ROS which undermines one of the body’s primary defenses. With \u0000advanced age, the inability to maintain this protective barrier appears to make \u0000us more susceptible to disease. ","PeriodicalId":18604,"journal":{"name":"Melatonin Research","volume":"114 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80198418","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Covid-19 deaths per million vary greatly between continents, with countries in South America having higher death rates even than Europe and North America, while Asia, Africa and Oceania have death rates which are only a fifth of those in South America. By analysing national level data on body weight, diet and latitude, we hypothesise and demonstrate that difference in the percentage of people with overweight (BMI > 25) may be the major factor that explains these differences in Covid-19 death rates. Meanwhile, within the group of countries where adult overweight is prevalent (i.e., where more than 50% of the population has BMI > 25), we hypothesise and demonstrate that latitude plays a role, with relatively lower death rates occurring in countries at lower latitudes. We further suggest that these relationships may be explained by two possible medical hypotheses relating to solar radiation: (1) In overweight people there is less penetration to important organs of near-infrared radiation (NIR) which stimulates production of subcellular melatonin, a strong anti-oxidizing factor and (2) In overweight people, fatty tissue holds much of the body´s 25(OH)D3 leaving less circulating in the blood stream. Several pathways have been proposed by other researchers to explain the link between Vitamin D deficiency and severity of Covid-19, but the possible link of Covid-19 outcome with NIR has not been explored. Latitude, of course, determines the amount of incoming NIR and as well as UV-B, which is the main stimulant for the body´s production of Vitamin D. It may well be that these two physiological processes operate simultaneously.
{"title":"A geographical approach to the development of hypotheses relating to Covid-19 death rates","authors":"M. Skutsch, R. Seheult, Jaime Loya","doi":"10.32794/mr112500132","DOIUrl":"https://doi.org/10.32794/mr112500132","url":null,"abstract":"Covid-19 deaths per million vary greatly between continents, with countries in South America having higher death rates even than Europe and North America, while Asia, Africa and Oceania have death rates which are only a fifth of those in South America. By analysing national level data on body weight, diet and latitude, we hypothesise and demonstrate that difference in the percentage of people with overweight (BMI > 25) may be the major factor that explains these differences in Covid-19 death rates. Meanwhile, within the group of countries where adult overweight is prevalent (i.e., where more than 50% of the population has BMI > 25), we hypothesise and demonstrate that latitude plays a role, with relatively lower death rates occurring in countries at lower latitudes. We further suggest that these relationships may be explained by two possible medical hypotheses relating to solar radiation: (1) In overweight people there is less penetration to important organs of near-infrared radiation (NIR) which stimulates production of subcellular melatonin, a strong anti-oxidizing factor and (2) In overweight people, fatty tissue holds much of the body´s 25(OH)D3 leaving less circulating in the blood stream. Several pathways have been proposed by other researchers to explain the link between Vitamin D deficiency and severity of Covid-19, but the possible link of Covid-19 outcome with NIR has not been explored. Latitude, of course, determines the amount of incoming NIR and as well as UV-B, which is the main stimulant for the body´s production of Vitamin D. It may well be that these two physiological processes operate simultaneously. ","PeriodicalId":18604,"journal":{"name":"Melatonin Research","volume":"20 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74774045","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
S. Süzen, M. C. Atayik, Hanif Sirinzade, Bita Entezari, H. Gurer-Orhan, U. Çakatay
Redox homeostasis and redox signaling are constituents of preservation of a normal physiological state. Whereas the equilibrium between oxidants and nucleophiles is conserved in redox homeostasis, oxidative stress promotes the formation of a radically altered redox state. It is known that modification of circadian clock may lead to severe alteration in redox balance. Melatonin [N-acetyl-5-methoxytryptamine, (MLT)] regulates numerous physiological functions including circadian rhythm, sleep-wake cycle, gonadal activity, redox homeostasis, neuroprotection, immune-modulation, and anticancer activity in organisms. Insufficient MLT production is closely related to development of aging process, tumorigenesis, visceral adiposity, neurodegenerative disorders, etc. Reactive oxygen species (ROS) are not intrinsically harmful or beneficial in cellular redox metabolism. Redox homeostasis is an integrative status for both of the hormetic response to ROS overproduction and subsequent redox signaling. MLT and its derivatives are traditionally classified as hormone-like substances. Their redox sensitive regulatory activity and direct interaction with intracellular ROS serve as second messenger in cell signaling. This review involves the role of redox homeostasis in the pathogenesis of age-related disorders and its relationship with MLT, therefore, targeting the circadian rhythm may propose new therapeutic approach for these disorders.
{"title":"Melatonin and redox homeostasis","authors":"S. Süzen, M. C. Atayik, Hanif Sirinzade, Bita Entezari, H. Gurer-Orhan, U. Çakatay","doi":"10.32794/mr112500134","DOIUrl":"https://doi.org/10.32794/mr112500134","url":null,"abstract":"Redox homeostasis and redox signaling are constituents of preservation of a normal physiological state. Whereas the equilibrium between oxidants and nucleophiles is conserved in redox homeostasis, oxidative stress promotes the formation of a radically altered redox state. It is known that modification of circadian clock may lead to severe alteration in redox balance. Melatonin [N-acetyl-5-methoxytryptamine, (MLT)] regulates numerous physiological functions including circadian rhythm, sleep-wake cycle, gonadal activity, redox homeostasis, neuroprotection, immune-modulation, and anticancer activity in organisms. Insufficient MLT production is closely related to development of aging process, tumorigenesis, visceral adiposity, neurodegenerative disorders, etc. Reactive oxygen species (ROS) are not intrinsically harmful or beneficial in cellular redox metabolism. Redox homeostasis is an integrative status for both of the hormetic response to ROS overproduction and subsequent redox signaling. MLT and its derivatives are traditionally classified as hormone-like substances. Their redox sensitive regulatory activity and direct interaction with intracellular ROS serve as second messenger in cell signaling. This review involves the role of redox homeostasis in the pathogenesis of age-related disorders and its relationship with MLT, therefore, targeting the circadian rhythm may propose new therapeutic approach for these disorders.","PeriodicalId":18604,"journal":{"name":"Melatonin Research","volume":"17 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81989683","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Manisha Mukhopadhyay, R. Majumder, Adrita Banerjee, D. Bandyopadhyay
Oxidative stress is a biological phenomenon described by decreased ability of the antioxidative system to neutralize excess reactive oxygen species (ROS). At low or moderate concentrations, ROS creates harmony in physiological functions but over production of ROS in long term can predisposes several chronic and neurodegenerative diseases such as coronary diseases, atherosclerosis, diabetes mellitus, hemolytic anemia, pulmonary diseases, neurodegenerative disorders, etc. The therapeutic use of antioxidants to control oxidative damage is a well-established phenomenon. In these aspects, melatonin and other classical antioxidant vitamins such as carotenoids, α-tocopherol, vitamin D, and ascorbic acid have gained enormous attention in the modern research area. In this review, we will discuss the comparative as well as the synergistic role of melatonin and other vitamins against stress-mediated disorders. Noteworthy, based on research evidence mentioned here we can recommend the combined use of melatonin and vitamins to alleviate the stress-induced toxicity in the broad spectrum.
{"title":"A comparative overview on the role of melatonin and vitamins as potential antioxidants against oxidative stress induced degenerative infirmities: An emerging concept","authors":"Manisha Mukhopadhyay, R. Majumder, Adrita Banerjee, D. Bandyopadhyay","doi":"10.32794/mr112500131","DOIUrl":"https://doi.org/10.32794/mr112500131","url":null,"abstract":"Oxidative stress is a biological phenomenon described by decreased ability of the antioxidative system to neutralize excess reactive oxygen species (ROS). At low or moderate concentrations, ROS creates harmony in physiological functions but over production of ROS in long term can predisposes several chronic and neurodegenerative diseases such as coronary diseases, atherosclerosis, diabetes mellitus, hemolytic anemia, pulmonary diseases, neurodegenerative disorders, etc. The therapeutic use of antioxidants to control oxidative damage is a well-established phenomenon. In these aspects, melatonin and other classical antioxidant vitamins such as carotenoids, α-tocopherol, vitamin D, and ascorbic acid have gained enormous attention in the modern research area. In this review, we will discuss the comparative as well as the synergistic role of melatonin and other vitamins against stress-mediated disorders. Noteworthy, based on research evidence mentioned here we can recommend the combined use of melatonin and vitamins to alleviate the stress-induced toxicity in the broad spectrum.","PeriodicalId":18604,"journal":{"name":"Melatonin Research","volume":"20 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82953370","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Timely reperfusion during myocardial infarction paradoxically leads to ischemia/reperfusion (I/R) injury. Mitochondrial quality control has emerged as a key participant in regulation of this process. The aims of this review are to briefly summarize current evidence for the role of mitochondrial quality control in I/R injury and to evaluate whether the cardioprotective actions of melatonin, a potent free radical scavenger and antioxidant, can be attributed to its effects on these processes. Using a variety of experimental models, in vivo and in vitro, melatonin-induced cardioprotection has been demonstrated to be associated with attenuation or reversal of the harmful effects of I/R on parameters of mitochondrial quality control as evidenced by (i) upregulation of mitochondrial fusion and inhibition of fission, particularly Drp1 expression and translocation from the cytosol to the mitochondria; (ii) changes in both the conventional and alternative mitophagy pathways. Melatonin significantly upregulates mitochondrial biogenesis and the expression of sirtuins 1, 3 and 6 and has a beneficial effect on mitochondrial-endoplasmic reticulum interaction in I/R. A novel observation is the ability of melatonin to stimulate intercellular transfer of mitochondria between damaged cells, although this has not yet been demonstrated in myocardial I/R. Melatonin treatment has profound effects on the diabetic heart: it reverses the significant reduction in function and inhibits the progression of diabetic cardiomyopathy which was associated with a significant effect on mitochondrial quality control, as evidenced by a reduction in fission. In summary, available evidence supports a major role for mitochondrial quality control in the beneficial actions of melatonin in the I/R heart.
{"title":"Mitochondrial dynamics in myocardial ischemia/reperfusion injury: Effects of melatonin","authors":"A. Lochner, M. Blignaut","doi":"10.32794/mr112500136","DOIUrl":"https://doi.org/10.32794/mr112500136","url":null,"abstract":"Timely reperfusion during myocardial infarction paradoxically leads to ischemia/reperfusion (I/R) injury. Mitochondrial quality control has emerged as a key participant in regulation of this process. The aims of this review are to briefly summarize current evidence for the role of mitochondrial quality control in I/R injury and to evaluate whether the cardioprotective actions of melatonin, a potent free radical scavenger and antioxidant, can be attributed to its effects on these processes. Using a variety of experimental models, in vivo and in vitro, melatonin-induced cardioprotection has been demonstrated to be associated with attenuation or reversal of the harmful effects of I/R on parameters of mitochondrial quality control as evidenced by (i) upregulation of mitochondrial fusion and inhibition of fission, particularly Drp1 expression and translocation from the cytosol to the mitochondria; (ii) changes in both the conventional and alternative mitophagy pathways. Melatonin significantly upregulates mitochondrial biogenesis and the expression of sirtuins 1, 3 and 6 and has a beneficial effect on mitochondrial-endoplasmic reticulum interaction in I/R. A novel observation is the ability of melatonin to stimulate intercellular transfer of mitochondria between damaged cells, although this has not yet been demonstrated in myocardial I/R. Melatonin treatment has profound effects on the diabetic heart: it reverses the significant reduction in function and inhibits the progression of diabetic cardiomyopathy which was associated with a significant effect on mitochondrial quality control, as evidenced by a reduction in fission. In summary, available evidence supports a major role for mitochondrial quality control in the beneficial actions of melatonin in the I/R heart.","PeriodicalId":18604,"journal":{"name":"Melatonin Research","volume":"7 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86324298","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
M. Datta, R. Majumder, A. Chattopadhyay, D. Bandyopadhyay
The renin-angiotensin system has emerged as a key modulator of cardiomyopathies, with both local and central effects on the cardiac tissue. With the increase in incidences of cardiac disorders worldwide, the roles of the renin-angiotensin system on the cardiomyopathies have been revealed by scientists. Recent reports suggest that this system might regulate the synthesis of melatonin. This has drawn the interest of scientists globally since melatonin has remarkable protective effects on cardiomyopathies caused by atherosclerosis, cardiac ischemia, and myocardial infarction. Thus, understanding the interactions of melatonin with various components of the renin-angiotensin system becomes a necessary step for devising a targeted therapy for the various cardiomyopathies. This review has summarized the major effects of various components of the renin-angiotensin system on the cardiac tissue and the interaction of this system with melatonin. The role of melatonin in mediating cardioprotective effects by inhibition of certain components of this system has also been discussed.
{"title":"Melatonin as a protective adjunct to the renin angiotensin system imbalance induced cardiovascular pathogenesis: A review","authors":"M. Datta, R. Majumder, A. Chattopadhyay, D. Bandyopadhyay","doi":"10.32794/mr112500126","DOIUrl":"https://doi.org/10.32794/mr112500126","url":null,"abstract":"The renin-angiotensin system has emerged as a key modulator of cardiomyopathies, with both local and central effects on the cardiac tissue. With the increase in incidences of cardiac disorders worldwide, the roles of the renin-angiotensin system on the cardiomyopathies have been revealed by scientists. Recent reports suggest that this system might regulate the synthesis of melatonin. This has drawn the interest of scientists globally since melatonin has remarkable protective effects on cardiomyopathies caused by atherosclerosis, cardiac ischemia, and myocardial infarction. Thus, understanding the interactions of melatonin with various components of the renin-angiotensin system becomes a necessary step for devising a targeted therapy for the various cardiomyopathies. This review has summarized the major effects of various components of the renin-angiotensin system on the cardiac tissue and the interaction of this system with melatonin. The role of melatonin in mediating cardioprotective effects by inhibition of certain components of this system has also been discussed.","PeriodicalId":18604,"journal":{"name":"Melatonin Research","volume":"5 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88148689","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Biological membranes are composed of a lipid bilayer with a heterogeneous structure and complex dynamics, both of which can be modulated by the presence of melatonin. The lateral heterogeneities in lipid bilayers, also known as lipid rafts, have unique molecular interactions with melatonin, which we review here. Specifically, we discuss the molecular-level, physicochemical influences of melatonin on dynamics of lipid rafts and their structural properties, including melatonin’s propensity to preserve the structural integrity of lipid rafts at different length scales, as revealed through a range of experimental techniques and theoretical approaches.
{"title":"Molecular interactions of melatonin with lipid rafts","authors":"D. Bolmatov, M. Lavrentovich, R. Reiter","doi":"10.32794/mr112500123","DOIUrl":"https://doi.org/10.32794/mr112500123","url":null,"abstract":"Biological membranes are composed of a lipid bilayer with a heterogeneous structure and complex dynamics, both of which can be modulated by the presence of melatonin. The lateral heterogeneities in lipid bilayers, also known as lipid rafts, have unique molecular interactions with melatonin, which we review here. Specifically, we discuss the molecular-level, physicochemical influences of melatonin on dynamics of lipid rafts and their structural properties, including melatonin’s propensity to preserve the structural integrity of lipid rafts at different length scales, as revealed through a range of experimental techniques and theoretical approaches.","PeriodicalId":18604,"journal":{"name":"Melatonin Research","volume":"144 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86754784","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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