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. 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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. 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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.
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.