Magnetic Fields / GSSG Cancer Research Results

MF, Magnetic Fields: Click to Expand ⟱
Features: Therapy
Magnetic Fields can be Static, or pulsed. The most common therapy is a pulsed magnetic field in the uT or mT range.
The main pathways affected are:
Calcium Signaling: -influence the activity of voltage-gated calcium channels.
Oxidative Stress and Reactive Oxygen Species (ROS) Pathways
Heat Shock Proteins (HSPs) and Cellular Stress Responses
Cell Proliferation and Growth Signaling: MAPK/ERK pathway.
Gene Expression and Epigenetic Modifications: NF-κB
Angiogenesis Pathways: VEGF (improving VEGF for normal cells)
PEMF was found to have a 2-fold increase in drug uptake compared to traditional electrochemotherapy in rat melanoma models

Pathways:
- most reports have ROS production increasing in cancer cells , while decreasing in normal cells.
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, GRP78↑, Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓, Prx,
- Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, Pro-Inflammatory Cytokines : NLRP3↓, IL-1β↓, TNF-α↓, IL-6↓, IL-8↓
- inhibit Growth/Metastases : TumMeta↓, TumCG↓, VEGF↓(mostly regulated up in normal cells),
- cause Cell cycle arrest : TumCCA↑,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, TNF-α↓,
- inhibits glycolysis /Warburg Effect and ATP depletion : HIF-1α↓, PKM2↓, GLUT1↓, LDH↓, HK2↓, PFKs↓, PDKs↓, ECAR↓, OXPHOS↓, GRP78↑, Glucose↓, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Notch↓, FGF↓, PDGF↓, EGFR↓, Integrins↓,
- Others: PI3K↓, AKT↓, STAT↓, Wnt↓, β-catenin↓, ERK↓, JNK, - SREBP (related to cholesterol).
- Synergies: chemo-sensitization, chemoProtective, cytoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Hepatoprotective, CardioProtective,

- Selectivity: Cancer Cells vs Normal Cells

Non-Static Magnetic Fields (AC / Pulsed / Oscillating MF)
Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 Reactive oxygen species (ROS) ↑ ROS (P→R); often sustained (G) ↑ ROS (P); ↔/↓ net ROS (R→G) P, R, G Upstream redox perturbation MF perturbs electron/radical dynamics: normal cells often adapt (ROS setpoint ↓), cancer cells less so
2 NRF2 antioxidant response ↔ / insufficient NRF2 induction (R→G) ↑ NRF2 activation (R→G) R, G Adaptive redox defense Explains mixed ROS direction in normal cells (initial ↑ then adaptive ↓)
3 Glutathione (GSH) homeostasis ↓ GSH (R→G) ↔ or transient ↓ (R) with recovery (G) R, G Redox buffering capacity GSH depletion reflects sustained oxidative load; recovery indicates successful adaptation
4 Superoxide dismutase (SOD) / antioxidant enzymes ↔ or inadequate enzyme upshift (G) ↑ SOD/GPx/CAT capacity (G) G Longer-term antioxidant remodeling Often the “endpoint” readout that correlates with ROS-normalization in normal tissue
5 Mitochondrial ETC / respiration ↓ ETC efficiency; ↑ electron leak (P→R) ↔ mild, reversible ETC perturbation (P→R) P, R Bioenergetic destabilization ETC perturbation is a mechanistic bridge between MF exposure and ROS/ΔΨm changes
6 Mitochondrial membrane potential (ΔΨm / MMP) ↓ ΔΨm (R); may progress (G) ↔ preserved or reversible dip (R) R, G Mitochondrial dysfunction thresholding ΔΨm loss typically follows ROS/ETC disruption rather than preceding it
7 Ca²⁺ signaling (VGCC / ER–mitochondria Ca²⁺ flux) ↑ dysregulated Ca²⁺ influx/transfer (P→R); overload may persist (G) ↑ transient Ca²⁺ signaling (P); homeostasis restored (R→G) P, R, G Stress signal amplification Ca²⁺ dysregulation links ROS/ETC perturbation to ER stress and mitochondrial dysfunction (amplifies ΔΨm loss and UPR commitment)
8 Mitochondrial permeability transition pore (MPTP) ↑ MPTP opening propensity (R); sustained opening possible (G) ↔ transient or closed (R→G) P, R, G Commitment point for mitochondrial failure MPTP opening integrates ROS, Ca²⁺ overload, and ΔΨm loss; acts as a threshold event converting reversible stress into irreversible mitochondrial dysfunction
9 ER stress / UPR ↑ ER stress (R); CHOP-commitment possible (G) ↑ adaptive UPR (R); resolves (G) R, G Proteostasis stress Often downstream of ROS + Ca²⁺ handling perturbations
10 DNA damage (oxidative) ↑ damage markers (R→G) ↔ or repaired (G) R, G Checkpoint pressure Generally secondary to ROS; interpret as stress consequence not “direct genotoxicity”
11 LDH / glycolytic flux ↓ glycolytic performance (R→G) ↔ flexible substrate switching (R→G) R, G Metabolic vulnerability Redox imbalance can destabilize high-rate glycolysis in cancer-biased contexts
12 Thioredoxin system (Trx / TrxR) ↓ functional reserve / overload (R→G) ↔ preserved capacity (G) R, G Parallel antioxidant system stress Useful when GSH-only does not explain redox phenotype 
Time-Scale Flag: TSF = P / R / G
  P: 0–30 min (physical / electron / radical effects)
  R: 30 min–3 hr (redox signaling & stress response)
  G: >3 hr (gene-regulatory adaptation)
MPTP: opening represents a mitochondrial commitment event integrating ROS and Ca²⁺ stress; sustained opening indicates irreversible bioenergetic failure.
GSSG, oxidized glutathione: Click to Expand ⟱
Source:
Type:
GSSG (oxidized glutathione) is a component of the cellular redox system rather than a protein or signaling molecule produced de novo. Its levels, often evaluated along with its reduced counterpart (GSH), serve as an important index of cellular oxidative stress and redox balance.

– GSSG is generated when glutathione (GSH) neutralizes reactive oxygen species (ROS) by donating electrons; in doing so, GSH is oxidized to GSSG.

– The GSH/GSSG ratio is a sensitive marker of the intracellular redox state. Under conditions of oxidative stress (commonly observed in many cancers), this ratio often shifts toward increased GSSG.

– Elevated GSSG levels (or an increased GSSG/GSH ratio) can indicate that cancer cells are under oxidative stress, which has implications both for cancer progression and for sensitivity to certain treatments.
Scientific Papers found: Click to Expand⟱
3463- MF,    Pulsed Electromagnetic Fields Alleviates Hepatic Oxidative Stress and Lipids Accumulation in db/db mice
- in-vivo, NA, NA
*hepatoP↑, *MDA↓, *GSSG↓, *GSH↑, *GPx↑, *antiOx↑, *SREBP1↓,

Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Total Targets: 0

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   GPx↑, 1,   GSH↑, 1,   GSSG↓, 1,   MDA↓, 1,  

Core Metabolism/Glycolysis ⓘ

SREBP1↓, 1,  

Functional Outcomes ⓘ

hepatoP↑, 1,  
Total Targets: 7

Scientific Paper Hit Count for: GSSG, oxidized glutathione
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:172  Target#:1212  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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