Magnetic Fields / Catalase 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↑">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.


Catalase, Catalase: Click to Expand ⟱
Source:
Type:
Caspases are a cysteine protease that speed up a chemical reaction via pointing their target substrates following an aspartic acid residue.1 They are grouped into apoptotic (caspase-2, 3, 6, 7, 8, 9 and 10) and inflammatory (caspase-1, 4, 5, 11 and 12) mediated caspases.
Caspase-1 may have both tumorigenic or antitumorigenic effects on cancer development and progression, but it depends on the type of inflammasome, methodology, and cancer.
Catalase is an enzyme found in nearly all living cells exposed to oxygen. Its primary role is to protect cells from oxidative damage by catalyzing the conversion of hydrogen peroxide (H₂O₂), a potentially damaging byproduct of metabolism, into water (H₂O) and oxygen (O₂). This detoxification process is crucial because excess H₂O₂ can lead to the formation of reactive oxygen species (ROS) that damage proteins, lipids, and DNA.

Catalase and Cancer
Oxidative Stress and Cancer:
Cancer cells often experience increased levels of oxidative stress due to rapid proliferation and metabolic changes. This stress can lead to DNA damage, promoting tumorigenesis.
Catalase helps mitigate oxidative stress, and its expression can influence the survival and proliferation of cancer cells.
Expression Levels in Different Cancers:
Overexpression: In some cancers, such as breast cancer and certain types of leukemia, catalase may be overexpressed. This overexpression can help cancer cells survive in oxidative environments, potentially leading to more aggressive tumor behavior.
Downregulation: Conversely, in other cancers, such as colorectal cancer, reduced catalase expression has been observed. This downregulation can lead to increased oxidative stress, contributing to tumor progression and metastasis.
Prognostic Implications:
Survival Rates: Studies have shown that high levels of catalase expression can be associated with poor prognosis in certain cancers, as it may enable cancer cells to resist apoptosis (programmed cell death) induced by oxidative stress.

Some types of cancer cells have been reported to exhibit lower catalase activity, possibly increasing their vulnerability to oxidative damage under certain conditions. This vulnerability has even been exploited in some therapeutic strategies (for example, approaches that generate excess H₂O₂ or other ROS specifically targeting cancer cells have been researched).


Scientific Papers found: Click to Expand⟱
356- AgNPs,  MF,    Anticancer and antibacterial potentials induced post short-term exposure to electromagnetic field and silver nanoparticles and related pathological and genetic alterations: in vitro study
- in-vitro, BC, MCF-7 - in-vitro, Bladder, HTB-22
Apoptosis↑, P53↑, iNOS↑, NF-kB↑, Bcl-2↓, ROS↑, SOD↑, TumCCA↑, eff↑, Catalase↑, other↑,
3457- MF,    Cellular stress response to extremely low‐frequency electromagnetic fields (ELF‐EMF): An explanation for controversial effects of ELF‐EMF on apoptosis
- Review, Var, NA
Apoptosis↑, H2O2↑, ROS↑, eff↑, eff↑, Ca+2↑, MAPK↑, *Catalase↑, *SOD1↑, *GPx1↑, *GPx4↑, *NRF2↑, TumAuto↑, ER Stress↑, HSPs↑, SIRT3↑, ChemoSen↑, UPR↑, other↑, PI3K↓, JNK↑, p38↑, eff↓, *toxicity?,
2253- MF,    Low-frequency pulsed electromagnetic field promotes functional recovery, reduces inflammation and oxidative stress, and enhances HSP70 expression following spinal cord injury
- in-vivo, Nor, NA
*Inflam↓, *TNF-α↓, *IL1β↓, *NF-kB↓, *iNOS↓, *ROS↓, Catalase↑, *SOD↑, *HSP70/HSPA5↑, *neuroP↑, *motorD↑, *antiOx↑,
4116- MF,    Low‑frequency pulsed electromagnetic field promotes functional recovery, reduces inflammation and oxidative stress, and enhances HSP70 expression following spinal cord injury
- in-vivo, NA, NA
*Inflam↓, *TNF-α↓, *IL1β↓, *iNOS↓, *ROS↓, *Catalase↑, *SOD↑, HSP70/HSPA5↑,
4111- MF,    Coupling of pulsed electromagnetic fields (PEMF) therapy to molecular grounds of the cell
- Review, Arthritis, NA
*Inflam↓, *Cartilage↑, *Pain↓, *QoL↑, *Dose↝, *VEGF↑, *NO↑, *TGF-β↑, *MMP9↓, *PGE2↑, *GPx3↑, *SOD2↑, *Catalase↑, *GSR↑, *Ca+2↑,
4102- MF,    Modulation of antioxidant enzyme gene expression by extremely low frequency electromagnetic field in post-stroke patients
- Human, Stroke, NA
*Catalase↑, *SOD1↑, *SOD2↑, *GPx1↑, *GPx4↑, *Dose↝,
5241- MF,    A review on the use of magnetic fields and ultrasound for non-invasive cancer treatment
- Review, Var, NA
other↑, BloodF↑, Glycolysis↓, ATP↓, VEGF↓, ROS↑, P-gp↓, Apoptosis↑, selectivity↑, Ca+2↑, Catalase↑,
4147- MF,    PEMFs Restore Mitochondrial and CREB/BDNF Signaling in Oxidatively Stressed PC12 Cells Targeting Neurodegeneration
- in-vitro, AD, PC12
*ROS↓, *Catalase↑, *MMP↑, *Casp3↓, *p‑ERK↓, *cAMP↑, *p‑CREB↑, *BDNF↑, *neuroP↑,
3498- MF,    Effect of Static Magnetic Field on Oxidant/Antioxidant Parameters in Cancerous and Noncancerous Human Gastric Tissues
- in-vitro, GC, NA
*SOD↑, *MDA↓, SOD↓, GPx↓, MDA↑, Catalase↑,
3484- MF,    Extremely low frequency pulsed electromagnetic fields cause antioxidative defense mechanisms in human osteoblasts via induction of •O2 − and H2O2
- in-vitro, Nor, NA
*GPx↑, *SOD2↑, *Catalase↑, *GSR↑, *ROS↓,
3567- MFrot,  MF,    The Effect of Extremely Low-Frequency Magnetic Field on Stroke Patients: A Systematic Review
- Review, Stroke, NA
*eff↑, *ROS↓, *Inflam↓, *cognitive↑, *Catalase↑, *SOD↑, *SOD1↑, *SOD2↑, *GPx1↑, *GPx4↑, *IL1β↑, *neuroP↑, *toxicity∅,
209- MFrot,  MF,    The effect of a rotating magnetic field on the antioxidant system in healthy volunteers - preliminary study
- Human, NA, NA
*SOD↑, *Catalase↑, *ROMO1↑, *MDA↓, *TAC↑, *ROS↓,

Showing Research Papers: 1 to 12 of 12

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 12

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress

Catalase↑, 4,   GPx↓, 1,   H2O2↑, 1,   MDA↑, 1,   ROS↑, 3,   SIRT3↑, 1,   SOD↓, 1,   SOD↑, 1,  

Mitochondria & Bioenergetics

ATP↓, 1,  

Core Metabolism/Glycolysis

Glycolysis↓, 1,  

Cell Death

Apoptosis↑, 3,   Bcl-2↓, 1,   iNOS↑, 1,   JNK↑, 1,   MAPK↑, 1,   p38↑, 1,  

Transcription & Epigenetics

other↑, 3,  

Protein Folding & ER Stress

ER Stress↑, 1,   HSP70/HSPA5↑, 1,   HSPs↑, 1,   UPR↑, 1,  

Autophagy & Lysosomes

TumAuto↑, 1,  

DNA Damage & Repair

P53↑, 1,  

Cell Cycle & Senescence

TumCCA↑, 1,  

Proliferation, Differentiation & Cell State

PI3K↓, 1,  

Migration

Ca+2↑, 2,  

Angiogenesis & Vasculature

VEGF↓, 1,  

Barriers & Transport

P-gp↓, 1,  

Immune & Inflammatory Signaling

NF-kB↑, 1,  

Drug Metabolism & Resistance

ChemoSen↑, 1,   eff↓, 1,   eff↑, 3,   selectivity↑, 1,  

Clinical Biomarkers

BloodF↑, 1,  
Total Targets: 34

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress

antiOx↑, 1,   Catalase↑, 8,   GPx↑, 1,   GPx1↑, 3,   GPx3↑, 1,   GPx4↑, 3,   GSR↑, 2,   MDA↓, 2,   NRF2↑, 1,   ROMO1↑, 1,   ROS↓, 6,   SOD↑, 5,   SOD1↑, 3,   SOD2↑, 4,   TAC↑, 1,  

Mitochondria & Bioenergetics

MMP↑, 1,  

Core Metabolism/Glycolysis

cAMP↑, 1,   p‑CREB↑, 1,  

Cell Death

Casp3↓, 1,   iNOS↓, 2,  

Protein Folding & ER Stress

HSP70/HSPA5↑, 1,  

Proliferation, Differentiation & Cell State

p‑ERK↓, 1,  

Migration

Ca+2↑, 1,   Cartilage↑, 1,   MMP9↓, 1,   TGF-β↑, 1,  

Angiogenesis & Vasculature

NO↑, 1,   VEGF↑, 1,  

Immune & Inflammatory Signaling

IL1β↓, 2,   IL1β↑, 1,   Inflam↓, 4,   NF-kB↓, 1,   PGE2↑, 1,   TNF-α↓, 2,  

Synaptic & Neurotransmission

BDNF↑, 1,  

Drug Metabolism & Resistance

Dose↝, 2,   eff↑, 1,  

Functional Outcomes

cognitive↑, 1,   motorD↑, 1,   neuroP↑, 3,   Pain↓, 1,   QoL↑, 1,   toxicity?, 1,   toxicity∅, 1,  
Total Targets: 44

Scientific Paper Hit Count for: Catalase, Catalase
12 Magnetic Fields
2 Magnetic Field Rotating
1 Silver-NanoParticles
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#:46  State#:%  Dir#:2
wNotes=0 sortOrder:rid,rpid

 

Home Page