地氟醚在神经科学氧化应激中的作用

Q4 Biochemistry, Genetics and Molecular Biology Journal of Cellular Neuroscience and Oxidative Stress Pub Date : 2018-08-18 DOI:10.37212/jcnos.610129
Mustafa Kütük
{"title":"地氟醚在神经科学氧化应激中的作用","authors":"Mustafa Kütük","doi":"10.37212/jcnos.610129","DOIUrl":null,"url":null,"abstract":"Oxidative stress in a neuron is induced by several  physiological and pathological processes. Within the  pathophysiological processes, ischemia-reperfusion  injury has major role in the neurons and brain, because  the neurons and brain are very sensitive to oxidative  stress as compared to other tissues due to their high  oxygen consumption rate and rich poly unsaturated fatty  acid content but low antioxidant levels. Results of  rodent studies indicated that exposure to volatile  anesthetics as a result of ischemia-reperfusion injury  can active leukocytes or alveolar macrophages, which,  in turn, release inflammatory mediators and reactive  oxygen species (ROS). This release of inflammatory  mediators, ischemia/reperfusion injury, and ROS has  been clearly demonstrated in generalized inflammatory  reactions involving the production of phagocytic cells  such as leucocytes and microglia. A common volatile  general anesthetic is desflurane and results of several  recent papers indicated that it  an increase oxidative  stress but can decrease antioxidant defense mechanisms  through ischemia/reperfusion injury mechanisms.  The excessive production of ROS is scavenged by  enzymatic and non-enzymatic antioxidants. Major  enzymatic antioxidants are vitamin A, vitamin C,  vitamin E, glutathione, alpha lipoic acid and melatonin.  Major non enzymatic antioxidants are glutathione  peroxidase (GSH-Px), superoxide dismutase (SOD) and  catalase (CAT). Superoxide radical is converted to  hydrogen peroxide by SOD enzyme and then the  hydrogen peroxide is converted to water by CAT and  GSH-Px enzymes. Results of papers indicated that the  CAT, GSH-Px, SOD, vitamin A, vitamin E and vitamin  C values were decreased in plasma and erythrocytes of  human and animals by desflurane anesthesia, but  oxidative stress levels were increased by desflurane  anesthesia (Allaouchiche et al. 2001; Ceylan et al. 2011;  Yalcin et al. 2013). In the oral presentation, I will  summarize the results of recent papers on oxidative  stress and antioxidants in human and rodents.  In conclusion, it seems that desflurane anesthesia  has oxidant effects through down-regulating the  enzymatic and non-enzymatic antioxidants but upregulating  of lipid peroxidation.","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":" ","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2018-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Role of desflurane on oxidative stress in neuroscience\",\"authors\":\"Mustafa Kütük\",\"doi\":\"10.37212/jcnos.610129\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Oxidative stress in a neuron is induced by several  physiological and pathological processes. Within the  pathophysiological processes, ischemia-reperfusion  injury has major role in the neurons and brain, because  the neurons and brain are very sensitive to oxidative  stress as compared to other tissues due to their high  oxygen consumption rate and rich poly unsaturated fatty  acid content but low antioxidant levels. Results of  rodent studies indicated that exposure to volatile  anesthetics as a result of ischemia-reperfusion injury  can active leukocytes or alveolar macrophages, which,  in turn, release inflammatory mediators and reactive  oxygen species (ROS). This release of inflammatory  mediators, ischemia/reperfusion injury, and ROS has  been clearly demonstrated in generalized inflammatory  reactions involving the production of phagocytic cells  such as leucocytes and microglia. A common volatile  general anesthetic is desflurane and results of several  recent papers indicated that it  an increase oxidative  stress but can decrease antioxidant defense mechanisms  through ischemia/reperfusion injury mechanisms.  The excessive production of ROS is scavenged by  enzymatic and non-enzymatic antioxidants. Major  enzymatic antioxidants are vitamin A, vitamin C,  vitamin E, glutathione, alpha lipoic acid and melatonin.  Major non enzymatic antioxidants are glutathione  peroxidase (GSH-Px), superoxide dismutase (SOD) and  catalase (CAT). Superoxide radical is converted to  hydrogen peroxide by SOD enzyme and then the  hydrogen peroxide is converted to water by CAT and  GSH-Px enzymes. Results of papers indicated that the  CAT, GSH-Px, SOD, vitamin A, vitamin E and vitamin  C values were decreased in plasma and erythrocytes of  human and animals by desflurane anesthesia, but  oxidative stress levels were increased by desflurane  anesthesia (Allaouchiche et al. 2001; Ceylan et al. 2011;  Yalcin et al. 2013). In the oral presentation, I will  summarize the results of recent papers on oxidative  stress and antioxidants in human and rodents.  In conclusion, it seems that desflurane anesthesia  has oxidant effects through down-regulating the  enzymatic and non-enzymatic antioxidants but upregulating  of lipid peroxidation.\",\"PeriodicalId\":37782,\"journal\":{\"name\":\"Journal of Cellular Neuroscience and Oxidative Stress\",\"volume\":\" \",\"pages\":\"\"},\"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.610129\",\"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.610129","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}
引用次数: 0

摘要

神经元的氧化应激是由几个生理和病理过程引起的。在病理生理过程中,缺血再灌注损伤在神经元和大脑中起着重要作用,因为与其他组织相比,神经元和大脑对氧化应激非常敏感,因为它们的耗氧量高,多不饱和脂肪酸含量丰富,但抗氧化水平低。啮齿动物研究结果表明,由于缺血再灌注损伤,暴露于挥发性麻醉剂可以激活白细胞或肺泡巨噬细胞,进而释放炎症介质和活性氧(ROS)。炎症介质、缺血/再灌注损伤和ROS的这种释放已在涉及吞噬细胞(如白细胞和小胶质细胞)产生的广泛炎症反应中得到明确证明。地氟醚是一种常见的挥发性全身麻醉剂,最近几篇论文的结果表明,它会增加氧化应激,但会通过缺血/再灌注损伤机制降低抗氧化防御机制。ROS的过量产生被酶和非酶抗氧化剂清除。主要的酶抗氧化剂是维生素A、维生素C、维生素E、谷胱甘肽、α-硫辛酸和褪黑素。主要的非酶抗氧化剂是谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)和过氧化氢酶(CAT)。超氧化物自由基通过SOD酶转化为过氧化氢,然后过氧化氢通过CAT和GSH-Px酶转化为水。论文结果表明,地氟醚麻醉降低了人和动物血浆和红细胞中的CAT、GSH-Px、SOD、维生素A、维生素E和维生素C值,但地氟醚麻醉增加了氧化应激水平(Allaouchhe等人,2001;Ceylan等人2011;Yalcin等人2013)。在口头陈述中,我将总结最近关于人类和啮齿动物氧化应激和抗氧化剂的论文的结果。总之,地氟醚麻醉似乎通过下调酶促和非酶促抗氧化剂而上调脂质过氧化而具有氧化作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
Role of desflurane on oxidative stress in neuroscience
Oxidative stress in a neuron is induced by several  physiological and pathological processes. Within the  pathophysiological processes, ischemia-reperfusion  injury has major role in the neurons and brain, because  the neurons and brain are very sensitive to oxidative  stress as compared to other tissues due to their high  oxygen consumption rate and rich poly unsaturated fatty  acid content but low antioxidant levels. Results of  rodent studies indicated that exposure to volatile  anesthetics as a result of ischemia-reperfusion injury  can active leukocytes or alveolar macrophages, which,  in turn, release inflammatory mediators and reactive  oxygen species (ROS). This release of inflammatory  mediators, ischemia/reperfusion injury, and ROS has  been clearly demonstrated in generalized inflammatory  reactions involving the production of phagocytic cells  such as leucocytes and microglia. A common volatile  general anesthetic is desflurane and results of several  recent papers indicated that it  an increase oxidative  stress but can decrease antioxidant defense mechanisms  through ischemia/reperfusion injury mechanisms.  The excessive production of ROS is scavenged by  enzymatic and non-enzymatic antioxidants. Major  enzymatic antioxidants are vitamin A, vitamin C,  vitamin E, glutathione, alpha lipoic acid and melatonin.  Major non enzymatic antioxidants are glutathione  peroxidase (GSH-Px), superoxide dismutase (SOD) and  catalase (CAT). Superoxide radical is converted to  hydrogen peroxide by SOD enzyme and then the  hydrogen peroxide is converted to water by CAT and  GSH-Px enzymes. Results of papers indicated that the  CAT, GSH-Px, SOD, vitamin A, vitamin E and vitamin  C values were decreased in plasma and erythrocytes of  human and animals by desflurane anesthesia, but  oxidative stress levels were increased by desflurane  anesthesia (Allaouchiche et al. 2001; Ceylan et al. 2011;  Yalcin et al. 2013). In the oral presentation, I will  summarize the results of recent papers on oxidative  stress and antioxidants in human and rodents.  In conclusion, it seems that desflurane anesthesia  has oxidant effects through down-regulating the  enzymatic and non-enzymatic antioxidants but upregulating  of lipid peroxidation.
求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Journal of Cellular Neuroscience and Oxidative Stress
Journal of Cellular Neuroscience and Oxidative Stress Biochemistry, Genetics and Molecular Biology-Biophysics
CiteScore
1.10
自引率
0.00%
发文量
8
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)
期刊最新文献
Circadian rhythms of antioxidant enzymes activity, clock, and inflammation factors are disrupted in the prefrontal cortex of aged rats. Potential targets for therapeutic strategies for a healthy aging. Neuroprotective Effect of Colocasia esculenta Var. Mentawai Corm Flour High-Fat Diet Fed Mice Protective effect of N-acetylcysteine on hippocampal ferroptosis in an experimental obesity model Regulatory role of phospholipase A2 inhibitor in oxidative stress and inflammation induced by an experimental mouse migraine model Fasting alters p75NTR and AgRP mRNA expression in rat olfactory bulb and hippocampus
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1