{"title":"褪黑素在创伤性脑损伤氧化应激中的作用","authors":"Y. Akyuva","doi":"10.37212/jcnos.610135","DOIUrl":null,"url":null,"abstract":"Oxidative stress occurs in the several physiological processes such as phagocytic activity and mitochondrial membrane functions. Oxidative stress is controlled by several enzymatic and non-enzymatic antioxidants. Traumatic brain injury is one of the most common causes of the mortalities. Secondary events occur after primary events like shearing of nerve cells and blood vessels, cause posttraumatic neurodegenerations with an increase in ROS and ROSmediated lipid peroxidation. Melatonin is a member of non-enzymatic antioxidant group. The protective effects of melatonin on traumatic brain injury have been shown in vivo and in vitro studies (Barlow et al. 2018). Also melatonin has been shown to counteract oxidative stress-induced pathophysiologic conditions like ischemia/reperfusion injury, neuronal excitotoxicity and chronic inflammation. Recently, it was reported that TBI-induced oxidative stress in experimental TBI was inhibited by the melatonin treatment (Senol and Naziroglu, 2014). In the oral presentation, I will review recent studies on traumatic brain injury in human and rodents. I concluded that the oxidative stress causes changes through activation of second messengers, which may lead to the pathology of TBI, although melatonin has protective effects on the pathology. It seems to that the exact relationship between melatonin and TBI still remain to be determined.","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2018-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Role of melatonin on oxidative stress in traumatic brain injury\",\"authors\":\"Y. Akyuva\",\"doi\":\"10.37212/jcnos.610135\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Oxidative stress occurs in the several physiological processes such as phagocytic activity and mitochondrial membrane functions. Oxidative stress is controlled by several enzymatic and non-enzymatic antioxidants. Traumatic brain injury is one of the most common causes of the mortalities. Secondary events occur after primary events like shearing of nerve cells and blood vessels, cause posttraumatic neurodegenerations with an increase in ROS and ROSmediated lipid peroxidation. Melatonin is a member of non-enzymatic antioxidant group. The protective effects of melatonin on traumatic brain injury have been shown in vivo and in vitro studies (Barlow et al. 2018). Also melatonin has been shown to counteract oxidative stress-induced pathophysiologic conditions like ischemia/reperfusion injury, neuronal excitotoxicity and chronic inflammation. Recently, it was reported that TBI-induced oxidative stress in experimental TBI was inhibited by the melatonin treatment (Senol and Naziroglu, 2014). In the oral presentation, I will review recent studies on traumatic brain injury in human and rodents. I concluded that the oxidative stress causes changes through activation of second messengers, which may lead to the pathology of TBI, although melatonin has protective effects on the pathology. It seems to that the exact relationship between melatonin and TBI still remain to be determined.\",\"PeriodicalId\":37782,\"journal\":{\"name\":\"Journal of Cellular Neuroscience and Oxidative Stress\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2018-08-18\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Cellular Neuroscience and Oxidative Stress\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.37212/jcnos.610135\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"Biochemistry, Genetics and Molecular Biology\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Cellular Neuroscience and Oxidative Stress","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.37212/jcnos.610135","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"Biochemistry, Genetics and Molecular Biology","Score":null,"Total":0}
Role of melatonin on oxidative stress in traumatic brain injury
Oxidative stress occurs in the several physiological processes such as phagocytic activity and mitochondrial membrane functions. Oxidative stress is controlled by several enzymatic and non-enzymatic antioxidants. Traumatic brain injury is one of the most common causes of the mortalities. Secondary events occur after primary events like shearing of nerve cells and blood vessels, cause posttraumatic neurodegenerations with an increase in ROS and ROSmediated lipid peroxidation. Melatonin is a member of non-enzymatic antioxidant group. The protective effects of melatonin on traumatic brain injury have been shown in vivo and in vitro studies (Barlow et al. 2018). Also melatonin has been shown to counteract oxidative stress-induced pathophysiologic conditions like ischemia/reperfusion injury, neuronal excitotoxicity and chronic inflammation. Recently, it was reported that TBI-induced oxidative stress in experimental TBI was inhibited by the melatonin treatment (Senol and Naziroglu, 2014). In the oral presentation, I will review recent studies on traumatic brain injury in human and rodents. I concluded that the oxidative stress causes changes through activation of second messengers, which may lead to the pathology of TBI, although melatonin has protective effects on the pathology. It seems to that the exact relationship between melatonin and TBI still remain to be determined.
期刊介绍:
Journal of Cellular Neuroscience and Oxidative Stress isan online journal that publishes original research articles, reviews and short reviews on themolecular basisofbiophysical,physiological and pharmacological processes thatregulate cellular function, and the control or alteration of these processesby theaction of receptors, neurotransmitters, second messengers, cation, anions,drugsor disease. Areas of particular interest are four topics. They are; 1. Ion Channels (Na+-K+Channels, Cl– channels, Ca2+channels, ADP-Ribose and metabolism of NAD+,Patch-Clamp applications) 2. Oxidative Stress (Antioxidant vitamins, antioxidant enzymes, metabolism of nitric oxide, oxidative stress, biophysics, biochemistry and physiology of free oxygen radicals) 3. Interaction Between Oxidative Stress and Ion Channels in Neuroscience (Effects of the oxidative stress on the activation of the voltage sensitive cation channels, effect of ADP-Ribose and NAD+ on activation of the cation channels which are sensitive to voltage, effect of the oxidative stress on activation of the TRP channels in neurodegenerative diseases such Parkinson’s and Alzheimer’s diseases) 4. Gene and Oxidative Stress (Gene abnormalities. Interaction between gene and free radicals. Gene anomalies and iron. Role of radiation and cancer on gene polymorphism)