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

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
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Abstract

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.

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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
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
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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.
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