Role of desflurane on oxidative stress in neuroscience

Q4 Biochemistry, Genetics and Molecular Biology
Mustafa Kütük
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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.
地氟醚在神经科学氧化应激中的作用
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。
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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)
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