Static Magnetic Stimulation Induces Changes in the Oxidative Status and Cell Viability Parameters in a Primary Culture Model of Astrocytes

Cell biochemistry and biophysics · 2021 · Harm · Low evidence

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HarmLow evidencePaper 1130

Study snapshot

PublicationCell biochemistry and biophysics · 2021

Study typein_vitro

Reported directionHarm

Evidence ratingLow

Abstract

Static Magnetic Stimulation Induces Changes in the Oxidative Status and Cell Viability Parameters in a Primary Culture Model of Astrocytes da Costa CC, Martins LAM, Koth AP, Ramos JMO, Guma FTCR, de Oliveira CM, Pedra NS, Fischer G, Helena ES, Gioda CR, Sanches PRS, Junior ASV, Soares MSP, Spanevello RM, Gamaro GD, de Souza ICC. Static Magnetic Stimulation Induces Changes in the Oxidative Status and Cell Viability Parameters in a Primary Culture Model of Astrocytes. Cell Biochem Biophys. 2021 Jun 27. doi: 10.1007/s12013-021-01015-7 Abstract Astrocytes play an important role in the central nervous system function and may contribute to brain plasticity response during static magnetic fields (SMF) brain therapy. However, most studies evaluate SMF stimulation in brain plasticity while few studies evaluate the consequences of SMF at the cellular level. Thus, we here evaluate the effects of SMF at 305 mT (medium-intensity) in a primary culture of healthy/normal cortical astrocytes obtained from neonatal (1 to 2-day-old) Wistar rats. After reaching confluence, cells were daily subjected to SMF stimulation for 5 min, 15 min, 30 min, and 40 min during 7 consecutive days. Oxidative stress parameters, cell cycle, cell viability, and mitochondrial function were analyzed. The antioxidant capacity was reduced in groups stimulated for 5 and 40 min. Although no difference was observed in the enzymatic activity of superoxide dismutase and catalase or the total thiol content, lipid peroxidation was increased in all stimulated groups. The cell cycle was changed after 40 min of SMF stimulation while 15, 30, and 40 min led cells to death by necrosis. Mitochondrial function was reduced after SMF stimulation, although imaging analysis did not reveal substantial changes in the mitochondrial network. Results mainly revealed that SMF compromised healthy astrocytes' oxidative status and viability. This finding reveals how important is to understand the SMF stimulation at the cellular level since this therapeutic approach has been largely used against neurological and psychiatric diseases. pubmed.ncbi.nlm.nih.gov

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AI evidence extraction

Structured fields below were generated from the paper’s abstract and metadata to make the evidence easier to inspect. Automated extraction may be incomplete or incorrect; verify important details against the original paper.

Study typein_vitro

Effect directionharm

PopulationPrimary culture of healthy/normal cortical astrocytes from neonatal (1–2-day-old) Wistar rats

Sample sizeNot supplied

Exposurestatic · Daily stimulation for 5, 15, 30, or 40 min over 7 consecutive days

Evidence strengthLowConfidence: 78% · Peer reviewed: yes

Main findings

Astrocytes exposed to 305 mT SMF showed reduced antioxidant capacity in the 5- and 40-min groups and increased lipid peroxidation in all stimulated groups, with no observed differences in superoxide dismutase, catalase, or total thiol content. Cell cycle changes were reported after 40 min of stimulation, and 15, 30, and 40 min exposures led to cell death by necrosis; mitochondrial function was reduced, while imaging did not show substantial changes in the mitochondrial network.

Outcomes measured

Oxidative stress parameters
Antioxidant capacity
Superoxide dismutase activity
Catalase activity
Total thiol content
Lipid peroxidation
Cell cycle
Cell viability
Necrosis
Mitochondrial function
Mitochondrial network (imaging)

Limitations

In vitro primary cell culture model (astrocytes)
Animal-derived cells (neonatal Wistar rats); may not generalize to humans
Sample size not reported in abstract
Exposure regimen limited to 305 mT and specific daily durations over 7 days

View raw extracted JSON

{
  "study_type": "in_vitro",
  "exposure": {
    "band": "static",
    "source": "static magnetic stimulation (SMF)",
    "frequency_mhz": null,
    "sar_wkg": null,
    "duration": "Daily stimulation for 5, 15, 30, or 40 min over 7 consecutive days"
  },
  "population": "Primary culture of healthy/normal cortical astrocytes from neonatal (1–2-day-old) Wistar rats",
  "sample_size": null,
  "outcomes": [
    "Oxidative stress parameters",
    "Antioxidant capacity",
    "Superoxide dismutase activity",
    "Catalase activity",
    "Total thiol content",
    "Lipid peroxidation",
    "Cell cycle",
    "Cell viability",
    "Necrosis",
    "Mitochondrial function",
    "Mitochondrial network (imaging)"
  ],
  "main_findings": "Astrocytes exposed to 305 mT SMF showed reduced antioxidant capacity in the 5- and 40-min groups and increased lipid peroxidation in all stimulated groups, with no observed differences in superoxide dismutase, catalase, or total thiol content. Cell cycle changes were reported after 40 min of stimulation, and 15, 30, and 40 min exposures led to cell death by necrosis; mitochondrial function was reduced, while imaging did not show substantial changes in the mitochondrial network.",
  "effect_direction": "harm",
  "limitations": [
    "In vitro primary cell culture model (astrocytes)",
    "Animal-derived cells (neonatal Wistar rats); may not generalize to humans",
    "Sample size not reported in abstract",
    "Exposure regimen limited to 305 mT and specific daily durations over 7 days"
  ],
  "evidence_strength": "low",
  "confidence": 0.78,
  "peer_reviewed_likely": "yes",
  "keywords": [
    "static magnetic field",
    "static magnetic stimulation",
    "SMF",
    "astrocytes",
    "oxidative stress",
    "lipid peroxidation",
    "cell viability",
    "necrosis",
    "mitochondrial function",
    "cell cycle",
    "305 mT"
  ],
  "suggested_hubs": [
    {
      "slug": "other",
      "weight": 0.2,
      "reason": "Static magnetic stimulation study in an in vitro astrocyte model; no specific portal hub indicated by the abstract."
    }
  ]
}

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AI-extracted fields are generated from the abstract and metadata and may be incomplete or incorrect. This material is for informational purposes and is not medical advice.

Identifiers and source

DOI: 10.1007/s12013-021-01015-7
PubMed: 34176101

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