The recently established relation between the metabolism of aromatic amino acids of yeast and the production of different bioactive molecules during fermentation opens up new and interesting research topics. Among these molecules, melatonin has drawn researchers’ attention in the last decade given its potential benefits for human health. This review summarizes melatonin production in fermented beverages, and conventional and current methods for detecting melatonin in yeast-derived samples. In addition, the role of melatonin in yeast is discussed and the biosynthetic pathway of melatonin is presented in Saccharomyces cerevisiae.
{"title":"Melatonin in yeast and fermented beverages: analytical tools for detection, physiological role and biosynthesis","authors":"Sara Muñiz-Calvo, Ricardo Bisquert, J. Guillamón","doi":"10.32794/mr11250053","DOIUrl":"https://doi.org/10.32794/mr11250053","url":null,"abstract":"The recently established relation between the metabolism of aromatic amino acids of yeast and the production of different bioactive molecules during fermentation opens up new and interesting research topics. Among these molecules, melatonin has drawn researchers’ attention in the last decade given its potential benefits for human health. This review summarizes melatonin production in fermented beverages, and conventional and current methods for detecting melatonin in yeast-derived samples. In addition, the role of melatonin in yeast is discussed and the biosynthetic pathway of melatonin is presented in Saccharomyces cerevisiae.","PeriodicalId":18604,"journal":{"name":"Melatonin Research","volume":"43 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88905629","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}
The revelation of adult brain exhibiting neurogenesis has established that the brain possesses great plasticity and that neurons could be spawned in the neurogenic zones where hippocampal adult neurogenesis attributes to learning and memory processes. With strong implications in brain functional homeostasis, aging and cognition, various aspects of adult neurogenesis reveal exuberant mechanistic associations thereby further aiding in facilitating the therapeutic approaches regarding the development of neurodegenerative processes in Alzheimer’s Disease (AD). Impaired neurogenesis has been significantly evident in AD with compromised hippocampal function and cognitive deficits. Melatonin the pineal indolamine augments neurogenesis and has been linked to AD development as its levels are compromised with disease progression. Here, in this review, we discuss and appraise the mechanisms via which melatonin regulates neurogenesis in pathophysiological conditions which would unravel the molecular basis in such conditions and its role in endogenous brain repair. Also, its components as key regulators of neural stem and progenitor cell proliferation and differentiation in the embryonic and adult brain would aid in accentuating the therapeutic implications of this indoleamine in line of prevention and treatment of AD.
{"title":"Role of melatonin in regulating neurogenesis: Implications for the neurodegenerative pathology and analogous therapeutics for Alzheimer’s disease","authors":"M. Shukla, Areechun Sotthibundhu, P. Govitrapong","doi":"10.32794/mr11250059","DOIUrl":"https://doi.org/10.32794/mr11250059","url":null,"abstract":"The revelation of adult brain exhibiting neurogenesis has established that the brain possesses great plasticity and that neurons could be spawned in the neurogenic zones where hippocampal adult neurogenesis attributes to learning and memory processes. With strong implications in brain functional homeostasis, aging and cognition, various aspects of adult neurogenesis reveal exuberant mechanistic associations thereby further aiding in facilitating the therapeutic approaches regarding the development of neurodegenerative processes in Alzheimer’s Disease (AD). Impaired neurogenesis has been significantly evident in AD with compromised hippocampal function and cognitive deficits. Melatonin the pineal indolamine augments neurogenesis and has been linked to AD development as its levels are compromised with disease progression. Here, in this review, we discuss and appraise the mechanisms via which melatonin regulates neurogenesis in pathophysiological conditions which would unravel the molecular basis in such conditions and its role in endogenous brain repair. Also, its components as key regulators of neural stem and progenitor cell proliferation and differentiation in the embryonic and adult brain would aid in accentuating the therapeutic implications of this indoleamine in line of prevention and treatment of AD. ","PeriodicalId":18604,"journal":{"name":"Melatonin Research","volume":"8 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78863142","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}
A. Madigan, Christopher Harris, Frank Bedon, A. Franks, K. Plummer
Melatonin is a secondary metabolite produced in all domains of life. Exogenous melatonin triggers defence mechanisms in plants that enhance abiotic stress tolerance. However, knowledge regarding the role of melatonin as a signal or an antioxidant in microbes is lacking. We investigated the in vitro growth responses of three phytopathogenic fungi, Sclerotinia sclerotiorum, Botrytis cinerea and Fusarium oxysporum f.sp. vasinfectum, to abiotic stress (2.5% ethanol with/without cold priming) under varying concentrations of melatonin. Melatonin at high concentrations (1000 – 2000 µM) partially restored fungal growth under stress, compared to controls, suggesting a role for melatonin in alleviating the impacts of stress exposure. Understanding how melatonin impacts fungal growth during stress conditions will be important for future applications using melatonin as a tool for crop protection.
{"title":"High doses of melatonin confer abiotic stress tolerance to phytopathogenic fungi grown in vitro","authors":"A. Madigan, Christopher Harris, Frank Bedon, A. Franks, K. Plummer","doi":"10.32794/mr11250056","DOIUrl":"https://doi.org/10.32794/mr11250056","url":null,"abstract":"Melatonin is a secondary metabolite produced in all domains of life. Exogenous melatonin triggers defence mechanisms in plants that enhance abiotic stress tolerance. However, knowledge regarding the role of melatonin as a signal or an antioxidant in microbes is lacking. We investigated the in vitro growth responses of three phytopathogenic fungi, Sclerotinia sclerotiorum, Botrytis cinerea and Fusarium oxysporum f.sp. vasinfectum, to abiotic stress (2.5% ethanol with/without cold priming) under varying concentrations of melatonin. Melatonin at high concentrations (1000 – 2000 µM) partially restored fungal growth under stress, compared to controls, suggesting a role for melatonin in alleviating the impacts of stress exposure. Understanding how melatonin impacts fungal growth during stress conditions will be important for future applications using melatonin as a tool for crop protection.","PeriodicalId":18604,"journal":{"name":"Melatonin Research","volume":"3 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80415890","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}
Adrita Banerjee, A. Chattopadhyay, D. Bandyopadhyay
Diabetes mellitus, one of the crucial epidemics of this country has snatched the sleep of mankind with a steep slope of 108 million in 1980 to more than 460 million in today’s world. The global statistics based on numerological information from World Health Organization (WHO) proposed alarmingly about 642 million affected individuals by 2040. Type 1 diabetes is due to damaged pancreatic β-cells while type 2 diabetes is a result of insulin insensitivity associated with hyperglycaemia. Hyperglycaemia is a principal symptom of diabetes. As a result, the circulatory erythrocytes [red blood cells (RBCs)] become the first and most vulnerable victims to confront such a stressful environment. The RBCs possess many components including haemoglobin, membrane proteins and lipids. They prefer to interact with glucose and form glycated haemoglobin and membrane phospholipid asymmetry which alters RBC adherence. These alterations trigger intracellular reactive oxygen species (ROS) formation and oxidative damage in diabetic erythrocytes. Melatonin, an indoleamine, ameliorates oxidative stress in various tissues and has the capacity of shielding erythrocytes from deleterious stress. A crucial relationship between melatonin and insulin indicates their interplay in occurrence of diabetes. Biorhythm entrained and receptor mediated action of melatonin on pancreatic β-cells in the context of hyperglycaemia are discussed for the first time in the review. Since melatonin protects against erythrocytes, as well as beneficial to diabetes, it is worthy to address proficiency of this indoleamine to the diabetic erythrocytes. In summary, this review has discussed the fostering role of melatonin in hyperglycaemia and encouraged further investigation related to the molecular pathways of melatonin on glucose metabolism.
{"title":"Biorhythmic and receptor mediated interplay between melatonin and insulin: its consequences on diabetic erythrocytes","authors":"Adrita Banerjee, A. Chattopadhyay, D. Bandyopadhyay","doi":"10.32794/mr12250060","DOIUrl":"https://doi.org/10.32794/mr12250060","url":null,"abstract":"Diabetes mellitus, one of the crucial epidemics of this country has snatched the sleep of mankind with a steep slope of 108 million in 1980 to more than 460 million in today’s world. The global statistics based on numerological information from World Health Organization (WHO) proposed alarmingly about 642 million affected individuals by 2040. Type 1 diabetes is due to damaged pancreatic β-cells while type 2 diabetes is a result of insulin insensitivity associated with hyperglycaemia. Hyperglycaemia is a principal symptom of diabetes. As a result, the circulatory erythrocytes [red blood cells (RBCs)] become the first and most vulnerable victims to confront such a stressful environment. The RBCs possess many components including haemoglobin, membrane proteins and lipids. They prefer to interact with glucose and form glycated haemoglobin and membrane phospholipid asymmetry which alters RBC adherence. These alterations trigger intracellular reactive oxygen species (ROS) formation and oxidative damage in diabetic erythrocytes. Melatonin, an indoleamine, ameliorates oxidative stress in various tissues and has the capacity of shielding erythrocytes from deleterious stress. A crucial relationship between melatonin and insulin indicates their interplay in occurrence of diabetes. Biorhythm entrained and receptor mediated action of melatonin on pancreatic β-cells in the context of hyperglycaemia are discussed for the first time in the review. Since melatonin protects against erythrocytes, as well as beneficial to diabetes, it is worthy to address proficiency of this indoleamine to the diabetic erythrocytes. In summary, this review has discussed the fostering role of melatonin in hyperglycaemia and encouraged further investigation related to the molecular pathways of melatonin on glucose metabolism. ","PeriodicalId":18604,"journal":{"name":"Melatonin Research","volume":"21 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78010360","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}
Felipe Teixeira Soares, Hiroyuki Otsuki Guimarães, Paulo Marcelo Silva da Silveira, Antonilde Marcelina Arruda de Sá, L. Sampaio
Benzo(e)pyrene is a cytotoxic chemical to the eyes, while neurohormone melatonin may exhibit protective effects on this cytotoxicity. In the current study, we have investigated the cytotoxic effects of benzo(e)pyrene on the chicken embryonic optic cups formation and whether melatonin supplementation protects chicken embryos against this xenobiotic toxicity. Fertilized chicken eggs were incubated for 48 h and then, they were divided into different groups. These groups included basal (without any treatment), control (distilled water), benzo(e)pyrene, melatonin and benzo(e)pyrene + melatonin groups, respectively. The 10 µl of distilled water or same volume of solution containing treatment compounds were injected into the air sac of the chicken egg. After an additional 18 h of incubation, the chicken embryos were excised and analyzed. The cytotoxicity was measured by a colorimetric whole chick embryo trypan blue assay. In embryos from basal, control and melatonin (0.01, 1 and 100 µM) groups, the frequency of the embryos with normal optic cups was 100% and had no increase in the embryonic cell death observed in post excision. In contrast, the frequency of normal optic cups in the benzo(e)pyrene (0.02 to 1200 µM) groups was significantly reduced (log IC50= -4.24 ± 0.02, R2= 0.98) with concentration-responsive manner. In addition, an increase in the embryonic cell death was also observed (log IC50 = -7.23 ± 0.28; R2 = 0.63). Melatonin treatment dose-responsively inhibited the benzo(e)pyrene-induced optic cups abnormality by 22.35 ± 4.06, 76.38 ± 3.30 and 100 % at the concentrations of 0.01, 1 and 100 µM, respectively. This same phenomenon was also observed in benzo(e)pyrene-induced embryonic cell death, i.e., melatonin suppressed the embryonic cell death by 16.67 ± 4.17, 54.17 ± 4.17 and 100 % with the abovementioned concentrations, respectively. Thus, melatonin supplementation injected into the chicken eggs protected against the benzo(e)pyrene embryotoxicity. Different pathways can be involved in melatonin’s protective effects.
{"title":"Melatonin supplementation protects against the benzo(e)pyrene cytotoxicity and optic cup formation disruption in chicken embryos","authors":"Felipe Teixeira Soares, Hiroyuki Otsuki Guimarães, Paulo Marcelo Silva da Silveira, Antonilde Marcelina Arruda de Sá, L. Sampaio","doi":"10.32794/mr11250058","DOIUrl":"https://doi.org/10.32794/mr11250058","url":null,"abstract":"Benzo(e)pyrene is a cytotoxic chemical to the \u0000eyes, while neurohormone melatonin may exhibit protective effects on this \u0000cytotoxicity. In the current study, we have investigated the cytotoxic effects \u0000of benzo(e)pyrene on the chicken embryonic optic cups formation and whether \u0000melatonin supplementation protects chicken embryos against this xenobiotic \u0000toxicity. Fertilized chicken eggs were incubated for 48 h and then, they were \u0000divided into different groups. These groups included basal (without any \u0000treatment), control (distilled water), benzo(e)pyrene, melatonin and \u0000benzo(e)pyrene + melatonin groups, respectively. The 10 µl of distilled water \u0000or same volume of solution containing treatment compounds were injected into \u0000the air sac of the chicken egg. After an additional 18 h of incubation, the \u0000chicken embryos were excised and analyzed. The cytotoxicity was measured by a \u0000colorimetric whole chick embryo trypan blue assay. In embryos from basal, \u0000control and melatonin (0.01, 1 and 100 µM) groups, the frequency of the embryos \u0000with normal optic cups was 100% and had no increase in the embryonic cell death \u0000observed in post excision. In contrast, the frequency of normal optic cups in the \u0000benzo(e)pyrene (0.02 to 1200 µM) groups was significantly reduced (log IC50= \u0000-4.24 ± 0.02, R2= 0.98) with concentration-responsive manner. In \u0000addition, an increase in the embryonic cell death was also observed (log IC50 = \u0000-7.23 ± 0.28; R2 = 0.63). Melatonin treatment dose-responsively inhibited \u0000the benzo(e)pyrene-induced optic cups abnormality by 22.35 ± 4.06, 76.38 ± 3.30 \u0000and 100 % at the concentrations of 0.01, 1 and 100 µM, respectively. This same \u0000phenomenon was also observed in benzo(e)pyrene-induced embryonic cell death, \u0000i.e., melatonin suppressed the embryonic cell death by 16.67 ± 4.17, 54.17 ± \u00004.17 and 100 % with the abovementioned concentrations, respectively. Thus, melatonin \u0000supplementation injected into the chicken eggs protected against the \u0000benzo(e)pyrene embryotoxicity. Different pathways can be involved in melatonin’s \u0000protective effects. ","PeriodicalId":18604,"journal":{"name":"Melatonin Research","volume":"21 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85711368","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}
Mariyah Hidayat, S. Khaliq, Abdullah Khurram, K. Lone
In the current study, we reported the beneficial effects of melatonin in preventing neonatal neuronal apoptosis induced by maternal hypothyroidism. During the gestation and early lactation stages, the mother rats were given propylthiouracil (PTU) to inhibit their thyroid gland activity which resulted in the increased serum TSH and reduced T4 levels. This maternal hypothyroidism caused neuronal apoptosis of their pups, particularly in the CA3 area of hippocampus. Melatonin administration preserved function of thyroid gland and significantly reduced the apoptosis. Further studies have uncovered the potentially protective mechanisms of melatonin, that is, as a mitochondrial targeted antioxidant, melatonin preserves the mitochondrial outer membrane, inhibits the release of cytochrome C from mitochondria to cytoplasm and down regulates the gene expressions of Bax, along with caspases 3 and 9. Thus, melatonin breaks the mitochondria related apoptotic pathway to suppress the neuronal apoptosis induced by the maternal hypothyroidism. Considering the limited remedies to effectively treat hypothyroidism associated neonatal brain damage, melatonin may provide an alternative method for this disorder.
{"title":"Protective effects of melatonin on mitochondrial injury and neonatal neuron apoptosis induced by maternal hypothyroidism","authors":"Mariyah Hidayat, S. Khaliq, Abdullah Khurram, K. Lone","doi":"10.32794/mr11250040","DOIUrl":"https://doi.org/10.32794/mr11250040","url":null,"abstract":"In the current study, we reported the beneficial effects of melatonin in preventing neonatal neuronal apoptosis induced by maternal hypothyroidism. During the gestation and early lactation stages, the mother rats were given propylthiouracil (PTU) to inhibit their thyroid gland activity which resulted in the increased serum TSH and reduced T4 levels. This maternal hypothyroidism caused neuronal apoptosis of their pups, particularly in the CA3 area of hippocampus. Melatonin administration preserved function of thyroid gland and significantly reduced the apoptosis. Further studies have uncovered the potentially protective mechanisms of melatonin, that is, as a mitochondrial targeted antioxidant, melatonin preserves the mitochondrial outer membrane, inhibits the release of cytochrome C from mitochondria to cytoplasm and down regulates the gene expressions of Bax, along with caspases 3 and 9. Thus, melatonin breaks the mitochondria related apoptotic pathway to suppress the neuronal apoptosis induced by the maternal hypothyroidism. Considering the limited remedies to effectively treat hypothyroidism associated neonatal brain damage, melatonin may provide an alternative method for this disorder.","PeriodicalId":18604,"journal":{"name":"Melatonin Research","volume":"10 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76644727","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}
J. Mayo, R. Cernuda, Isabel Quirós, Pablo Luque Rodríguez, Joselyn García, D. Hevia, R. Sainz
Oncogenes alters metabolic pathways while the resulted metabolites, in turn, modifies the expression and production of oncogenes or tumor suppressors. Metabolic reprogramming has been considered as a consequence of oncogenes’ activity more than a phenotypic change of cancer cells. Currently, three different metabolic alterations for cancer cells, i.e. an increased ability to acquire nutrients, preferred metabolic pathways or differentiation pathways, have been described. Melatonin is a molecule which has been extensively investigated since it was discovered more than 60 years ago. From the aggregation of melanophores to antioxidant chain reactions, melatonin has been proposed to be an important molecule affecting the physiology of mammals but also the biology of unicellular organisms. Thus, the decrease in melatonin synthesis in humans with age has been related to several diseases including neurodegeneration and cancer. For many years, it has been believed that melatonin crosses biological membranes easily to exert its functions. However, this notion has been challenged by recent discovery that majority of melatonin might cross biological membranes through glucose transporters. This initial observation has generated a new important idea about melatonin’s function, that is, the membrane transportation of melatonin and glucose by the same transporter in cancer cells would be a new promising mechanism of this indole by either reprogramming glucose metabolism, impeding nutrients uptake or assigning preferred metabolic pathways in cancer cells. In this review, we will focus the role of melatonin as an antiproliferative agent, and its connection with metabolic changes due to melatonin competition with glucose.
{"title":"Understanding the role of melatonin in cancer metabolism","authors":"J. Mayo, R. Cernuda, Isabel Quirós, Pablo Luque Rodríguez, Joselyn García, D. Hevia, R. Sainz","doi":"10.32794/11250032","DOIUrl":"https://doi.org/10.32794/11250032","url":null,"abstract":"Oncogenes alters metabolic pathways while the resulted metabolites, in turn, \u0000modifies the expression and production of oncogenes or tumor suppressors. Metabolic \u0000reprogramming has been considered as a consequence of oncogenes’ activity more \u0000than a phenotypic change of cancer cells. Currently, three different metabolic \u0000alterations for cancer cells, i.e. an increased ability to acquire nutrients, \u0000preferred metabolic pathways or differentiation pathways, have been described. \u0000Melatonin is a molecule which has been extensively investigated since it was \u0000discovered more than 60 years ago. From the aggregation of melanophores to \u0000antioxidant chain reactions, melatonin has been proposed to be an important \u0000molecule affecting the physiology of mammals but also the biology of \u0000unicellular organisms. Thus, the decrease in melatonin synthesis in humans with \u0000age has been related to several diseases including neurodegeneration and \u0000cancer. For many years, it has been believed that melatonin crosses biological \u0000membranes easily to exert its functions. However, this notion has been \u0000challenged by recent discovery that majority of melatonin might cross biological \u0000membranes through glucose transporters. This initial observation has generated a \u0000new important idea about melatonin’s function, that is, the membrane transportation \u0000of melatonin and glucose by the same transporter in cancer cells would be a new \u0000promising mechanism of this indole by either reprogramming glucose metabolism, \u0000impeding nutrients uptake or assigning preferred metabolic pathways in cancer \u0000cells. In this review, we will focus the role of melatonin as an \u0000antiproliferative agent, and its connection with metabolic changes due to \u0000melatonin competition with glucose.","PeriodicalId":18604,"journal":{"name":"Melatonin Research","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88761606","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}
G. Bose, A. Ghosh, A. Chattopadhyay, P. Pal, D. Bandyopadhyay
High fat diet (HFD) has been implicated as an independent risk factor for cardiovascular diseases since the second half of the last century. The HFD causes various pathogeneses and progressions of cardiovascular diseases. The oxidative stress and pro-inflammatory reactions induced by the HFD are probably the major risk factors of myocardial damage. In this review we highlight the roles of different dietary fats on cardiovascular diseases and the protective effects of melatonin as a potent antioxidant and anti-inflammation molecule on the pathology induced by HFD. The focus will be given to the molecular mechanisms. The protective effects of melatonin on HFD induced myocardial damage are mediated by multiple pathways. These include that melatonin suppresses the oxidative stress, preserves the normal fat and glucose metabolisms and reduces the pro-inflammatory reactions. Melatonin downregulates the expressions of pro-inflammatory genes of TLR4, NF-κB and NLRP3-Caspase1 but upregulates the expressions of anti-inflammatory genes of Sirt3, CTRP3 and RISK. All of these render melatonin as a powerful protector against cardiovascular diseases caused by the HFD. This review suggests that melatonin can be used as a therapeutic agent in this specific condition.
{"title":"Melatonin as a potential therapeutic molecule against myocardial damage caused by high fat diet (HFD)","authors":"G. Bose, A. Ghosh, A. Chattopadhyay, P. Pal, D. Bandyopadhyay","doi":"10.32794/mr11250030","DOIUrl":"https://doi.org/10.32794/mr11250030","url":null,"abstract":" High fat diet (HFD) has been implicated as an independent risk factor for cardiovascular diseases since the second half of the last century. The HFD causes various pathogeneses and progressions of cardiovascular diseases. The oxidative stress and pro-inflammatory reactions induced by the HFD are probably the major risk factors of myocardial damage. In this review we highlight the roles of different dietary fats on cardiovascular diseases and the protective effects of melatonin as a potent antioxidant and anti-inflammation molecule on the pathology induced by HFD. The focus will be given to the molecular mechanisms. The protective effects of melatonin on HFD induced myocardial damage are mediated by multiple pathways. These include that melatonin suppresses the oxidative stress, preserves the normal fat and glucose metabolisms and reduces the pro-inflammatory reactions. Melatonin downregulates the expressions of pro-inflammatory genes of TLR4, NF-κB and NLRP3-Caspase1 but upregulates the expressions of anti-inflammatory genes of Sirt3, CTRP3 and RISK. All of these render melatonin as a powerful protector against cardiovascular diseases caused by the HFD. This review suggests that melatonin can be used as a therapeutic agent in this specific condition. ","PeriodicalId":18604,"journal":{"name":"Melatonin Research","volume":"25 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90152083","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}
R. Majumder, M. Datta, P. Pal, B. Bhattacharjee, A. Chattopadhyay, D. Bandyopadhyay
Current study explores the potential mechanisms of melatonin on cadmium-induced spleen tissue injury of goat. Spleen tissues were incubated with different concentrations (50, 100, 200, 400 and 600 µM) of cadmium acetate (Cd), respectively and the lipid peroxidation of the tissue was measured. It was found that Cd at the level of 400 µM induced maximum spleen damage among other concentrations. Thus, Cd 400 µM was selected to examine whether melatonin treatment can protect against this damage. The results showed that Cd increased the oxidative stress in the spleen tissue either by elevating pro-oxidant enzymes, or, by suppressing the variety of antioxidant enzymes and thus, to increase the intracellular reactive oxygen species (ROS). Melatonin treatment at the concentrations of 0.25, 0.5 and 1 mM significantly reduced all these alterations, respectively. At the level of cellular organelles, Cd caused mitochondrial morphological and functional injuries. These include mitochondrial surface distortion and inhibitions of glycolytic, Krebs cycle, and respiratory chain enzymes. Melatonin at a concentration of 0.5 mM almost completely preserved Cd induced mitochondrial pathological alterations. Cd pollution is a cause of serious health hazard world wide, particularly in the developing areas and currently, there is no specific remedy for Cd toxicities. The results suggest that melatonin is a promising therapeutic agent to combat Cd-induced oxidative stress and it deserves further investigation clinically.
{"title":"Protective mechanisms of melatonin on caprine spleen injury induced by cadmium (Cd): an in vitro study","authors":"R. Majumder, M. Datta, P. Pal, B. Bhattacharjee, A. Chattopadhyay, D. Bandyopadhyay","doi":"10.32794/11250031","DOIUrl":"https://doi.org/10.32794/11250031","url":null,"abstract":"Current study explores \u0000the potential mechanisms of melatonin on cadmium-induced spleen tissue injury \u0000of goat. Spleen tissues were incubated with different concentrations (50, 100, \u0000200, 400 and 600 µM) of cadmium acetate (Cd), respectively and the lipid \u0000peroxidation of the tissue was measured. It was found that Cd at the level of \u0000400 µM induced maximum spleen damage among other concentrations. Thus, Cd 400 \u0000µM was selected to examine whether melatonin treatment can protect against this \u0000damage. The results showed that Cd increased the oxidative stress in the spleen \u0000tissue either by elevating pro-oxidant enzymes, or, by suppressing the variety \u0000of antioxidant enzymes and thus, to increase the intracellular reactive oxygen \u0000species (ROS). Melatonin treatment at the concentrations of 0.25, 0.5 and 1 mM \u0000significantly reduced all these alterations, respectively. At the level of \u0000cellular organelles, Cd caused mitochondrial morphological and functional \u0000injuries. These include mitochondrial surface distortion and inhibitions of glycolytic, \u0000Krebs cycle, and respiratory chain enzymes. Melatonin at a concentration of 0.5 \u0000mM almost completely preserved Cd induced mitochondrial pathological \u0000alterations. Cd \u0000pollution is a cause of serious health hazard world wide, particularly in the \u0000developing areas and currently, there is no specific remedy for Cd toxicities. \u0000The results suggest that melatonin is a promising therapeutic agent to \u0000combat Cd-induced oxidative stress and it deserves further investigation \u0000clinically. ","PeriodicalId":18604,"journal":{"name":"Melatonin Research","volume":"46 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81553770","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}
R. Reiter, Ramaswamy Sharma, Q. Ma, S. Rosales‐Corral, D. Acuña-Castroviejo, G. Escames
This review presents a hypothesis to explain the role of melatonin in regulating glucose metabolism in cancer cells. Many cancer cells use cytosolic glycolysis (the Warburg effect) to produce energy (ATP). Under these conditions, glucose is primarily converted to lactate which is released into the blood in large quantities. The Warburg effect gives cancer cells advantages in terms of enhanced macromolecule synthesis required for accelerated cellular proliferation, reduced cellular apoptosis which enhances tumor biomass and a greater likelihood of metastasis. Based on available data, high circulating melatonin levels at night serve as a signal for breast cancer cells to switch from cytosolic glycolysis to mitochondrial glucose oxidation and oxidative phosphorylation for ATP production. In this situation, melatonin promotes the synthesis of acetyl-CoA from pyruvate; we speculate that melatonin does this by inhibiting the mitochondrial enzyme pyruvate dehydrogenase kinase (PDK) which normally inhibits pyruvate dehydrogenase complex (PDC), the enzyme that controls the pyruvate to acetyl-CoA conversion. Acetyl-CoA has several important functions in the mitochondria; it feeds into the citric acid cycle which improves oxidative phosphorylation and, additionally, it is a necessary co-factor for the rate limiting enzyme, arylalkylamine N-acetyltransferase, in mitochondrial melatonin synthesis. When breast cancer cells are using cytosolic glycolysis (during the day) they are of the cancer phenotype; at night when they are using mitochondria to produce ATP via oxidative phosphorylation, they have a normal cell phenotype. If this day:night difference in tumor cell metabolism is common in other cancers, it indicates that these tumor cells are only cancerous part of the time. We also speculate that high nighttime melatonin levels also reverse the insensitivity of tumors to chemotherapy.
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