静态磁场降低细胞内 ROS 水平并保护细胞免受过氧化物引发的损伤建议过氧化氢酶发挥的作用

IF 2.9 3区 医学 Q2 NEUROSCIENCES Neurotoxicity Research Pub Date : 2023-12-14 DOI:10.1007/s12640-023-00679-8
Emilli Caroline Garcia Frachini, Jean Bezerra Silva, Barbara Fornaciari, Maurício S. Baptista, Henning Ulrich, Denise Freitas Siqueira Petri
{"title":"静态磁场降低细胞内 ROS 水平并保护细胞免受过氧化物引发的损伤建议过氧化氢酶发挥的作用","authors":"Emilli Caroline Garcia Frachini, Jean Bezerra Silva, Barbara Fornaciari, Maurício S. Baptista, Henning Ulrich, Denise Freitas Siqueira Petri","doi":"10.1007/s12640-023-00679-8","DOIUrl":null,"url":null,"abstract":"<p>A feature in neurodegenerative disorders is the loss of neurons, caused by several factors including oxidative stress induced by reactive oxygen species (ROS). In this work, static magnetic field (SMF) was applied in vitro to evaluate its effect on the viability, proliferation, and migration of human neuroblastoma SH-SY5Y cells, and on the toxicity induced by hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>), tert-butyl hydroperoxide (tBHP), H<sub>2</sub>O<sub>2</sub>/sodium azide (NaN<sub>3</sub>) and photosensitized oxidations by photodynamic therapy (PDT) photosensitizers. The SMF increased almost twofold the cell expression of the proliferation biomarker Ki-67 compared to control cells after 7 days of exposure. Exposure to SMF accelerated the wound healing of scratched cell monolayers and significantly reduced the H<sub>2</sub>O<sub>2</sub>-induced and the tBHP-induced cell deaths. Interestingly, SMF was able to revert the effects of NaN<sub>3</sub> (a catalase inhibitor), suggesting an increased activity of catalase under the influence of the magnetic field. In agreement with this hypothesis, SMF significantly reduced the oxidation of DCF-H2, indicating a lower level of intracellular ROS. When the redox imbalance was triggered through photosensitized oxidation, no protection was observed. This observation aligns with the proposed role of catalase in cellular proctetion under SMF. Exposition to SMF should be further validated in vitro and in vivo as a potential therapeutic approach for neurodegenerative disorders.</p><h3 data-test=\"abstract-sub-heading\">Graphical Abstract</h3>","PeriodicalId":19193,"journal":{"name":"Neurotoxicity Research","volume":"4 1","pages":""},"PeriodicalIF":2.9000,"publicationDate":"2023-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Static Magnetic Field Reduces Intracellular ROS Levels and Protects Cells Against Peroxide-Induced Damage: Suggested Roles for Catalase\",\"authors\":\"Emilli Caroline Garcia Frachini, Jean Bezerra Silva, Barbara Fornaciari, Maurício S. Baptista, Henning Ulrich, Denise Freitas Siqueira Petri\",\"doi\":\"10.1007/s12640-023-00679-8\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p>A feature in neurodegenerative disorders is the loss of neurons, caused by several factors including oxidative stress induced by reactive oxygen species (ROS). In this work, static magnetic field (SMF) was applied in vitro to evaluate its effect on the viability, proliferation, and migration of human neuroblastoma SH-SY5Y cells, and on the toxicity induced by hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>), tert-butyl hydroperoxide (tBHP), H<sub>2</sub>O<sub>2</sub>/sodium azide (NaN<sub>3</sub>) and photosensitized oxidations by photodynamic therapy (PDT) photosensitizers. The SMF increased almost twofold the cell expression of the proliferation biomarker Ki-67 compared to control cells after 7 days of exposure. Exposure to SMF accelerated the wound healing of scratched cell monolayers and significantly reduced the H<sub>2</sub>O<sub>2</sub>-induced and the tBHP-induced cell deaths. Interestingly, SMF was able to revert the effects of NaN<sub>3</sub> (a catalase inhibitor), suggesting an increased activity of catalase under the influence of the magnetic field. In agreement with this hypothesis, SMF significantly reduced the oxidation of DCF-H2, indicating a lower level of intracellular ROS. When the redox imbalance was triggered through photosensitized oxidation, no protection was observed. This observation aligns with the proposed role of catalase in cellular proctetion under SMF. Exposition to SMF should be further validated in vitro and in vivo as a potential therapeutic approach for neurodegenerative disorders.</p><h3 data-test=\\\"abstract-sub-heading\\\">Graphical Abstract</h3>\",\"PeriodicalId\":19193,\"journal\":{\"name\":\"Neurotoxicity Research\",\"volume\":\"4 1\",\"pages\":\"\"},\"PeriodicalIF\":2.9000,\"publicationDate\":\"2023-12-14\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Neurotoxicity Research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1007/s12640-023-00679-8\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"NEUROSCIENCES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neurotoxicity Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s12640-023-00679-8","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
引用次数: 0

摘要

神经退行性疾病的一个特征是神经元的丧失,这是由多种因素引起的,包括活性氧(ROS)诱导的氧化应激。在体外实验中,研究了静磁场(SMF)对人神经母细胞瘤SH-SY5Y细胞活力、增殖和迁移的影响,以及过氧化氢(H2O2)、过氧化叔丁基氢(thbhp)、H2O2/氮化钠(NaN3)和光动力治疗(PDT)光敏剂致光敏氧化的毒性。与对照细胞相比,暴露7天后,SMF细胞增殖生物标志物Ki-67的细胞表达量几乎增加了两倍。SMF暴露加速了划伤细胞单层的伤口愈合,显著减少h2o2诱导和thbp诱导的细胞死亡。有趣的是,SMF能够恢复NaN3(一种过氧化氢酶抑制剂)的作用,这表明在磁场的影响下过氧化氢酶的活性增加。与这一假设一致,SMF显著降低了DCF-H2的氧化,表明细胞内ROS水平较低。当通过光敏氧化触发氧化还原失衡时,没有观察到保护作用。这一观察结果与过氧化氢酶在SMF下细胞保护中的作用一致。暴露于SMF作为神经退行性疾病的潜在治疗方法,应该在体外和体内进一步验证。图形抽象
本文章由计算机程序翻译,如有差异,请以英文原文为准。

摘要图片

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
Static Magnetic Field Reduces Intracellular ROS Levels and Protects Cells Against Peroxide-Induced Damage: Suggested Roles for Catalase

A feature in neurodegenerative disorders is the loss of neurons, caused by several factors including oxidative stress induced by reactive oxygen species (ROS). In this work, static magnetic field (SMF) was applied in vitro to evaluate its effect on the viability, proliferation, and migration of human neuroblastoma SH-SY5Y cells, and on the toxicity induced by hydrogen peroxide (H2O2), tert-butyl hydroperoxide (tBHP), H2O2/sodium azide (NaN3) and photosensitized oxidations by photodynamic therapy (PDT) photosensitizers. The SMF increased almost twofold the cell expression of the proliferation biomarker Ki-67 compared to control cells after 7 days of exposure. Exposure to SMF accelerated the wound healing of scratched cell monolayers and significantly reduced the H2O2-induced and the tBHP-induced cell deaths. Interestingly, SMF was able to revert the effects of NaN3 (a catalase inhibitor), suggesting an increased activity of catalase under the influence of the magnetic field. In agreement with this hypothesis, SMF significantly reduced the oxidation of DCF-H2, indicating a lower level of intracellular ROS. When the redox imbalance was triggered through photosensitized oxidation, no protection was observed. This observation aligns with the proposed role of catalase in cellular proctetion under SMF. Exposition to SMF should be further validated in vitro and in vivo as a potential therapeutic approach for neurodegenerative disorders.

Graphical Abstract

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
Neurotoxicity Research
Neurotoxicity Research 医学-神经科学
CiteScore
7.70
自引率
5.40%
发文量
164
审稿时长
6-12 weeks
期刊介绍: Neurotoxicity Research is an international, interdisciplinary broad-based journal for reporting both basic and clinical research on classical neurotoxicity effects and mechanisms associated with neurodegeneration, necrosis, neuronal apoptosis, nerve regeneration, neurotrophin mechanisms, and topics related to these themes. Published papers have focused on: NEURODEGENERATION and INJURY Neuropathologies Neuronal apoptosis Neuronal necrosis Neural death processes (anatomical, histochemical, neurochemical) Neurodegenerative Disorders Neural Effects of Substances of Abuse NERVE REGENERATION and RESPONSES TO INJURY Neural Adaptations Neurotrophin mechanisms and actions NEURO(CYTO)TOXICITY PROCESSES and NEUROPROTECTION Excitatory amino acids Neurotoxins, endogenous and synthetic Reactive oxygen (nitrogen) species Neuroprotection by endogenous and exogenous agents Papers on related themes are welcome.
期刊最新文献
No Benefit of 3% Hypertonic Saline Following Experimental Intracerebral Hemorrhage. How is Excitotoxicity Being Modelled in iPSC-Derived Neurons? Impact of 5-Lipoxygenase Deficiency on Dopamine-Mediated Behavioral Responses. Pharmacology of Adenosine A1 Receptor Agonist in a Humanized Esterase Mouse Seizure Model Following Soman Intoxication. The Role of Vitamin C on ATPases Activities in Monosodium Glutamate-Induced Oxidative Stress in Rat Striatum and Cerebellum.
×
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