Database Query Results : Magnetic Fields, , selectivity

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


selectivity, selectivity: Click to Expand ⟱
Source:
Type:
The selectivity of cancer products (such as chemotherapeutic agents, targeted therapies, immunotherapies, and novel cancer drugs) refers to their ability to affect cancer cells preferentially over normal, healthy cells. High selectivity is important because it can lead to better patient outcomes by reducing side effects and minimizing damage to normal tissues.

Achieving high selectivity in cancer treatment is crucial for improving patient outcomes. It relies on pinpointing molecular differences between cancerous and normal cells, designing drugs or delivery systems that exploit these differences, and overcoming intrinsic challenges like tumor heterogeneity and resistance

Factors that affect selectivity:
1. Ability of Cancer cells to preferentially absorb a product/drug
-EPR-enhanced permeability and retention of cancer cells
-nanoparticle formations/carriers may target cancer cells over normal cells
-Liposomal formations. Also negatively/positively charged affects absorbtion

2. Product/drug effect may be different for normal vs cancer cells
- hypoxia
- transition metal content levels (iron/copper) change probability of fenton reaction.
- pH levels
- antiOxidant levels and defense levels

3. Bio-availability
Scientific Papers found: Click to Expand⟱
2018- CAP,  MF,    Capsaicin: Effects on the Pathogenesis of Hepatocellular Carcinoma
- Review, HCC, NA
TRPV1↑, Capsaicin is an agonist for transient receptor potential cation channel subfamily V member 1 (TRPV1)
eff↑, It is noteworthy that capsaicin binding to the TRPV1 receptor may be increased using a static magnetic field (SMF), thus enhancing the anti-cancer effect of capsaicin on HepG2 (human hepatoblastoma cell line) cells through caspase-3 apoptosis
Akt↓, capsaicin can regulate autophagy by inhibiting the Akt/mTOR
mTOR↓,
p‑STAT3↑, Capsaicin can upregulate the activity of the signal transducer and activator of transcription 3 (p-STAT3)
MMP2↑, increase of the expression of MMP-2
ER Stress↑, capsaicin may induce apoptosis through endoplasmic reticulum (ER) stress
Ca+2↑, and the subsequent ER release of Ca2+
ROS↑, Capsaicin-induced ROS generation
selectivity↑, On the other hand, an excess of capsaicin is cytotoxic on HepG2 cells, and normal hepatocytes to a smaller extent, by collapse of the mitochondrial membrane potential with ROS formation
MMP↓,
eff↑, combination of capsaicin and sorafenib demonstrated significant anticarcinogenic properties on LM3 HCC cells, restricting tumor cell growth

526- MF,    Inhibition of Cancer Cell Growth by Exposure to a Specific Time-Varying Electromagnetic Field Involves T-Type Calcium Channels
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MCF-7 - in-vitro, Pca, HeLa - vitro+vivo, Melanoma, B16-BL6 - in-vitro, Nor, HEK293
TumCG↓, Exposure to Thomas-EMF inhibited tumour growth in mice
Ca+2↑, exposure of malignant cells to Thomas-EMF for > 15 min promoted Ca2+ influx
selectivity↑, but did not effect non-malignant cells
*Ca+2∅, only malignant cells showed enhanced Ca2+ uptake following exposure to Thomas-EMF.
ROS↑, EMF-dependent increases in reactive oxygen species, rapid influx of Ca2+, or activation of specific signaling pathway
HSP70/HSPA5↑, Some studies have shown increased expression of HSP70, a marker of cellular stress responses, in response to EMF exposures
AntiCan↑, These observations suggest that the Thomas-EMF could provide a potential anti-cancer therapy.

532- MF,    A 50 Hz magnetic field influences the viability of breast cancer cells 96 h after exposure
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MCF-7 - in-vitro, Nor, MCF10
TumCP↓,
MMP↓, MCF-7 breast cancer cells showed a significant decrease in ΔΨM compared with control cells after 4 and 24 h of exposure only when ΔΨM was analyzed at 96 h
ROS↑, All three breast cell lines analyzed showed an increase in ROS levels compared to those in nonexposed cells after both 4 h and 24 h of 1.0 mT ELF-MF exposure
eff↝, short-term exposure (4–8 h, 0.1 mT and 1.0 mT) led to an increase in viability in breast cancer cells, while long and high exposure (24 h, 1.0 mT) led to a decrease in viability and proliferation in all cell lines.
selectivity↑, Conversely, we did not observe significant differences in MCF-10A live cell number after 0.1 mT ELF-MF cell exposure

534- MF,    Effect of extremely low frequency electromagnetic field parameters on the proliferation of human breast cancer
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231 - in-vivo, Nor, MCF10
Ca+2↑, Exposure of the MDA-MB-231 cells to ELF-EMF also increased the fluorescence of the Ca2+ dye, FLUO-4 (AM) within 30 min, indicating an increase in Ca2+ influx compared to the control
Apoptosis↑,
eff↝, The cell viability increased with increases in the applied frequency. The ELF-EMF at 7.83Hz± 0.3 Hz showed the strongest inhibition of cell viability among the three frequency conditions
eff↑, The cells exposed to 6 h switching at 7.83Hz±0.3 Hz and 1mT for 2 consecutive days showed the strongest decrease in cell viability (from 100% to 40%)
selectivity↑, By contrast, the viability of the noncancerous M10 cells was unchanged by exposure to the T1 conditions,
eff↝, These differences in Ca2+ uptake behavior in the malignant cells could explain why MCF-7 and MDA-MB-231 cells are more sensitive than non-malignant M10 breast cells to EMF exposure.
eff↝, Our study also showed a clear window of vulnerability of cancer cells to ELF-EMF and that greater doses and magnitudes would be not unnecessarily better

3465- MF,    Magnetic fields and angiogenesis
- Review, Var, NA
angioG↓, angiogenesis of tumor tissues can be inhibited by both static and dynamic magnetic fields at animal level.
*angioG↑, In contrast, long-term or high-intensity static magnetic field treatment of non-tumor tissue seems to be able to promote angiogenesis at animal level.
selectivity↑,
Ca+2↝, People speculate that magnetic field may regulate angiogenesis by affecting multiple signal transduction pathways including the calcium signaling pathway.
ROS↝, studies showing that other molecules could be involved in this process, including ROS (reactive oxygen species, ROS), ERK and membrane-bound receptors

2260- MF,    Alternative magnetic field exposure suppresses tumor growth via metabolic reprogramming
- in-vitro, GBM, U87MG - in-vitro, GBM, LN229 - in-vivo, NA, NA
TumCP↓, proliferation of human glioblastoma multiforme (GBM) cells (U87 and LN229) was inhibited upon exposure to AMF within a specific narrow frequency range, including around 227 kHz.
TumCG↓, daily exposure to AMF for 30 min over 21 days significantly suppressed tumor growth and prolonged overall survival
OS↑,
ROS↑, This effect was associated with heightened reactive oxygen species (ROS) production and increased manganese superoxide dismutase (MnSOD) expression.
SOD2↑,
eff↓, anti-cancer efficacy of AMF was diminished by either a mitochondrial complex IV inhibitor or a ROS scavenger.
ECAR↓, decrease in the extracellular acidification rate (ECAR) and an increase in the oxygen consumption rate (OCR).
OCR↑,
selectivity↑, This suggests that AMF-induced metabolic reprogramming occurs in GBM cells but not in normal cells. Furthermore, in cancer cells, AMF decreased ECAR and increased OCR, while there were no changes in normal cells.
*toxicity∅, did not affect non-cancerous human cells [normal human astrocyte (NHA), human cardiac fibroblast (HCF), human umbilical vein endothelial cells (HUVEC)].
TumVol↓, The results showed a significant treatment effect, as assessed by tumor volume, after conducting AMF treatment five times a week for 2 weeks
PGC-1α↑, Corresponding to the rise in ROS, there was also a time-dependent increase in PGC1α protein expression post-AMF exposure
OXPHOS↑, enhancing mitochondrial oxidative phosphorylation (OXPHOS), leading to increased ROS production
Glycolysis↓, metabolic mode of cancer cells to shift from glycolysis, characteristic of cancer cells, toward OXPHOS, which is more typical of normal cells.
PKM2↓, We extracted proteins that changed commonly in U87 and LN229 cells. Among the individual proteins related to metabolism, pyruvate kinase M2 (PKM2) was found to be inhibited in both.

2261- MF,    Tumor-specific inhibition with magnetic field
- in-vitro, Nor, GP-293 - in-vitro, Liver, HepG2 - in-vitro, Lung, A549
ROS↑, It enhances cell oxidative stress response and regulates apoptosis signaling pathway, changing intracellular Ca2+ concentration to induce apoptosis
Ca+2↓,
Apoptosis↑,
*selectivity↑, No signicant difference was found between the exposed 293T cell count versus the control group without magnetic exposure on the third day of exposure.
TumCG↓, Hepg2, A549 cell counts were signicantly lower than the unexposed control groups (the highest inhibition rate of Hepg2 was about 18%, and the highest inhibition rate of A549 was about 30%).
*i-Ca+2↓, Normal cells 293T showed a significant decrease in intracellular free calcium ion,
i-Ca+2↑, solid tumor cells showed no signicant change, while suspended tumor showed a slight increase in calcium ion

2244- MF,    Little strokes fell big oaks: The use of weak magnetic fields and reactive oxygen species to fight cancer
- Review, Var, NA
RPM↑, WEMFs affect multiple cellular processes through mechanisms such as the radical pair mechanism (RPM), which alters reactive oxygen species (ROS) levels, mitochondrial function, and glycolysis
Glycolysis∅, WEMF parallel to the magnetic field (does not enchance glycolysis)
ROS↑, WEMF can augment this effect by enhancing mitochondrial respiration, which increases ROS levels within cancer cells. This augmentation makes cancer cells more susceptible to treatment by promoting oxidative stress that can lead to apoptosis
ChemoSen↑, Chemotherapeutic agents, such as doxorubicin, primarily exert their effects by generating ROS to induce cell death. WEMF can augment this effect by enhancing mitochondrial respiration, which increases ROS levels
RadioS↑, Similarly, WEMF can enhance the efficacy of radiation therapy by increasing ROS production and sensitizing cancer cells to radiation-induced DNA damage
selectivity↑, primary advantage of WEMF is its non-invasive, non-ionizing nature, which minimizes collateral damage to healthy tissue.

2237- MF,    The Effect of Pulsed Electromagnetic Field Stimulation of Live Cells on Intracellular Ca2+ Dynamics Changes Notably Involving Ion Channels
- in-vitro, AML, KG-1 - in-vitro, Nor, HUVECs
Ca+2↑, In both the KG-1 and HUVECs, PEMF stimulation resulted in enhanced Ca2+ influx
selectivity↑, response of [Ca2+]i due to PEMF stimulation appeared in the opposite direction in HUVECs.
*Inflam↓, PEMF also effected a decrease in the inflammatory cytokines TNF-alpha and NFkB in macrophage-like cells [9]. Although these studies suggest that PEMF is effective in wound healing and at attenuating inflammation
*TNF-α↓,
*NF-kB↓,
*Ca+2↓, ATP-sensitive Ca2+ influx and ER Ca2+ release of HUVECs were decreased by PEMP stimulation.

512- MF,    Pulsed Electromagnetic Fields (PEMFs) Trigger Cell Death and Senescence in Cancer Cells
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231 - in-vitro, Nor, FF95
TumCP↓,
*toxicity↓, PEMF application decreases the proliferation rate and viability of breast cancer cells while having the opposite effect on normal fibroblasts.
ChemoSen↑, ELF-PEMFs, as a pathology treatment approach, they have mainly been used as a complementary type of therapy, coupled with chemo-/radiotherapy,
RadioS↑,
selectivity↑, Collectively, these data indicate that PEMF irradiation exhibited not only anti-cancer properties but also beneficial effects for the normal cells.

507- MF,    Effects of extremely low frequency electromagnetic fields on the tumor cell inhibition and the possible mechanism
- in-vitro, Liver, HepG2 - in-vitro, Lung, A549 - in-vitro, Nor, GP-293
MMP↓,
TumCG↓,
ROS↑, key to tumor growth inhibition
*Ca+2↓, Normal 293 T cells showed a significant decrease in the intracellular free calcium ion concentration.
Ca+2↑, The solid tumor cells showed no significant change, while the suspended tumor cells showed a slight increase in the calcium ion concentration
selectivity↑,
i-pH↑, In addition, the intracellular pH of A549 cells increased under the magnetic field.

501- MF,    Low Intensity and Frequency Pulsed Electromagnetic Fields Selectively Impair Breast Cancer Cell Viability
- in-vitro, BC, MCF-7 - in-vitro, Nor, MCF10
Apoptosis↑, MCF10 cells were slightly benefitted by these same PEMF parameters ****
*toxicity↓, harmless to non-malignant cell types
ChemoSen↑, adjuvant treatment to more traditional chemo- and radiotherapies with the aim of reducing their dosage, mitigating any harmful secondary side effects and enhancing patient prognosis.
chemoP↑,
selectivity↑, killing of MCF7 cells : 3 mT peak-to-peak magnitude, at a pulse frequency of 20 Hz and duration of exposure of only 60 minutes per day. By stark contrast, this same pulsing paradigm (cytotoxic to MCF-7s) was innocuous to normal MCF-10 breast cells
DNAdam↑, Once again, 60 minutes of 3 mT PEMFs for three consecutive days gave the greatest DNA damage in MCF7 cancer cells.

4092- MF,    Mechanisms and therapeutic effectiveness of pulsed electromagnetic field therapy in oncology
- Review, Var, NA
Apoptosis↑, 20 Hz; 3 mT, 60mins/day PEMFs increased apoptosis in MCF7 cells but had no effect on MCF10 cells
selectivity↑,
ROS↑, 50 Hz, 0.1–1.0 mT) for 30 min, and long‐term PEMF: undifferentiated PC12 cells increased ROS levels and decreased catalase activity
Catalase↓,
TumVol↓, 1 Hz, 100 mT, Mice exposed for 60 and 180 min daily showed a 30% and 70% tumor reduction
angioG↓, PEMFs inhibit angiogenesis in tumor tissues, suppressing tumor vascularization and reducing tumor growth, as shown by in vivo studies

3478- MF,    One Month of Brief Weekly Magnetic Field Therapy Enhances the Anticancer Potential of Female Human Sera: Randomized Double-Blind Pilot Study
- Trial, BC, NA - in-vitro, BC, MCF-7 - in-vitro, Nor, C2C12
TumCP↓, Female sera from the magnetic therapy group (n = 12) reduced breast cancer cell proliferation (16.1%), migration (11.8%) and invasion (28.2%) and reduced the levels of key EMT markers relative to the control sera
TumCMig↓,
TumCI↓,
*toxicity∅, The provision of week 5 or week 8 PEMF sera to MCF10A cells did not alter their viability, being comparable to that observed with the control sera (
TGF-β↓, The week 8 PEMF sera resulted in the significant downregulation of (A) TGFβR2, (B) TWIST, (C) SNAI1, (D) SNAI2 (Slug), (E) β-catenin and (F) Vimentin protein expressions, when compared to week 8 control sera
Twist↓,
Slug↓,
β-catenin/ZEB1↓,
Vim↓,
p‑SMAD2↓, Week 5 PEMF sera primarily reduced the phosphorylation of SMAD 2/3 as well as the expression of TWIST protein expression.
p‑SMAD3↓,
angioG↓, Week 8 PEMF-plasma showed significant reductions in angiogenic biomarkers, including Angiopoietin-2, BMP-9, Endoglin, PLGF, VEGF-A, and VEGF-D
VEGF↓,
selectivity↑, PEMF sera did not adversely alter the growth of non-malignant cells such as MCF10A (breast epithelial) and C2C12 (myogenic).
LIF↑, Similarly, LIF (leukemia inhibitory factor) was upregulated one week after the final PEMF treatment.

3480- MF,    Cellular and Molecular Effects of Magnetic Fields
- Review, NA, NA
ROS↑, 50 Hz, 1 mT for 24/48/72 h SH-SY5Y (neuroblastoma Significantly increased ROS levels
*Ca+2↑, There is experimental proof that extremely low-frequency (ELF-MF) magnetic fields interact with Ca2+ channels, leading to increased Ca2+ efflux
*Inflam↓, PEMF stimulates the anti-inflammatory response of mesenchymal stem cells.
*Akt↓, nasopharyngeal carcinoma cell line. Potentially, these alterations were caused by inhibition of the Akt/mTOR signaling pathway
*mTOR↓,
selectivity↑, Ashdown and colleagues observed disruptions in the human lung cancer cell line after PMF (20 mT) exposure; in comparison, normal cells were insensitive to PMF
*memory↑, Ahmed and colleagues proved that PMF has an impact on the hippocampus, the brain region responsible for spatial orientation and memory acquisition.
*MMPs↑, In wound closure, epithelial cells, connective tissue cells, and immune cells, which promote collagen production, matrix metalloproteinase activity, growth factor release (e.g., VEGF, FGF, PDGF, TNF, HGF, and IL-1), and inflammatory environment pro
*VEGF↑,
*FGF↑,
*PDGF↑,
*TNF-α↑,
*HGF/c-Met↑,
*IL1↑,

2258- MFrot,  MF,    EXTH-68. ONCOMAGNETIC TREATMENT SELECTIVELY KILLS GLIOMA CANCER CELLS BY INDUCING OXIDATIVE STRESS AND DNA DAMAGE
- in-vitro, GBM, GBM - in-vitro, Nor, SVGp12
TumVol↓, GBM patient reversed the progression of his recurrent tumor causing >30% reduction in its contrast-enhanced volume within 4 weeks of treatment
OS↑, Mice with implanted mouse glioma cells in their brains also showed marked reduction in tumor size, increased survival (p< 0.05, n = 10)
γH2AX↑, higher DNA damage (g-H2AX foci) after sOMF treatment with a whole-body stimulation method developed by us
DNAdam↑,
selectivity↑, Normal mice exposed to sOMF for 4 months had no adverse effects on the brain and other organs
ROS↑, sOMF markedly increased reactive oxygen species (ROS) levels in cancer cells leading to the selective death of these cells, while sparing normal neurons and astrocytes
TumCD↑,
eff↑, sOMF exposure for just 2 h resulted in >40% loss of surviving GBM and DIPG cell colonies detected by clonogenic cell survival assay, similar to that produced by 2 Gy radiation dose.
eff↓, This loss was rescued by the antioxidant Trolox

2259- MFrot,  MF,    Method and apparatus for oncomagnetic treatment
- in-vitro, GBM, NA
MMP↓, Oncomagnetic patent Fig 2
Bcl-2↓,
BAX↑,
Bak↑,
Cyt‑c↑,
Casp3↑, caspase staining rises progressively until after 30 min most of the cells fluoresce positive for caspase, revealing activation of this enzyme
Casp9↑,
DNAdam↑,
ROS↑, applying the oscillating magnetic field to the tissue increases the production of reactive oxygen species (ROS )
lactateProd↑,
Apoptosis↑,
MPT↑, opening of the mitochondrial membrane permeability transition pore
*selectivity↑, repetitive magnetic stimulation has shown decreased apoptosis in non -cancerous cells .
eff↑, oncomagnetic therapy may be performed in conjunction with other forms of therapy such as with chemotherapy, other forms of radiative therapy, with drugs and prescriptions, etc
MMP↓, OMF which in turn produces rapidly fluctuating or sustained depolarizations of the mitochondrial membrane potential (MMP) in the tissue .
selectivity↑, Because normal cells have a larger amount of mitochondria, have lower demand for ATP, and are not under stress, disruption of electron flow and small amount of ROS formation and MMP depolarization does not trigger apoptosis
TCA?, decrease in Krebs cycle metabolites
H2O2↑, increase in peroxide levels in GBM cells following stimulation by the system 100 using a rotating magnet
eff↑, combine the administration of BHB , or acetoacetate , or free fatty acid, or branched chain amino acid, or cryptochrome agonist , or MGMT inhibitor, or DNA alkylating agent, or DNA methylating agent, and OMF as a more effective treatment of cancer
*antiOx↑, upregulation of antioxidant mechanisms due to the application of OMFs further protects non -cancerous cells from any ROS -mediated apoptosis
H2O2↑, The experiments showed rapid increases in the levels of superoxide and H2O2 in GBM cells
eff↓, To test whether cell death is caused by the OMF - induced increase in ROS , a potent antioxidant Trolox was used to counteract it, while measuring the decrease in GBM cell count due to 4 h exposure to OMF.
GSH/GSSG↓, GSH/GSSG ratio almost exactly half that seen in control cells
*toxicity∅, No Cytotoxic Effect in Normal Cells
OS↑, OMF -Induced Prolongation of Survival in a Mouse Xenograft Model of GBM

205- MFrot,  MF,    Intermittent F-actin Perturbations by Magnetic Fields Inhibit Breast Cancer Metastasis
- vitro+vivo, BC, MDA-MB-231
OS↑, 31-46% prolonged survival
F-actin↓, decrease F-actin formation in vitro and in vivo
TumCI↓,
TumCMig↓, >4.5hrs
Rho↓,
selectivity↑, F-actin in noncancerous breast cells is much less sensitive than that in breast cancer cells, which indicate that the normal cells in our human bodies are less likely to be agitated by these magnetic fields.

186- MFrot,  MF,    Selective induction of rapid cytotoxic effect in glioblastoma cells by oscillating magnetic fields
- in-vitro, GBM, GBM - in-vitro, Lung, NA
mt-ROS↑,
Casp3↑,
selectivity↑, OMF induces highly selective cell death of patient derived GBM cells associated with activation of caspase 3, while leaving normal tissue cells undamaged
TumCD↑,

187- MFrot,  MF,    Method for noninvasive whole-body stimulation with spinning oscillating magnetic fields and its safety in mice
- in-vivo, GBM, NA
selectivity↑, Our in vitro experiments demonstrated selective cancer cell death while sparing normal cells by sOMF-induced increase in intracellular reactive oxygen species (ROS) levels due to magnetic perturbation of mitochondrial electron transport.
ROS↑,
*ROS∅,
*toxicity∅, no significant adverse effects of chronic or acute sOMF stimulation on the health, behavior, electrocardiographic and electroencephalographic activities, hematologic profile, and brain and other tissue and organ morphology of treated mice

184- MFrot,  MF,    Rotating Magnetic Fields Inhibit Mitochondrial Respiration, Promote Oxidative Stress and Produce Loss of Mitochondrial Integrity in Cancer Cells
- in-vitro, GBM, GBM
ROS↑, sOMF
mitResp↓, Inhibit Mitochondrial Respiration
mtDam↑, Produce Loss of Mitochondrial Integrity
Dose↝, Repeated intermittent sOMF was applied for 2 hours at a specific frequency, in the 200-300 Hz frequency range, with on-off epochs of 250 or 500 ms duration.
MMP?, ROS generation has been shown to be driven, in part, by elevated mitochondrial membrane chemiosmotic potential (ΔΨ) and ubiquinol (QH2)
OCR↓, Immediately after cessation of field rotation we observe a loss of mitochondrial integrity (labeled LMI), with a very rapid increase in O2 consumption
mt-H2O2↑, We have previously demonstrated that sOMF treatment of cells generates superoxide/hydrogen peroxide in the mitochondrial matrix
eff↓, we repeated the same experiment in the presence of Trolox, which protects thiols from ROS oxidation (47). sOMF treatment of RLM in State 3u pre-treated with Trolox (15 μM), show minimal inhibition,
SDH↓, SDH Inhibition by sOMF in State 3u RLM Is Caused by ROS Generation
Thiols↓, suggest that thiol oxidation in SDH may result from sOMF.
GSH↓, Glutathione in the mitochondrial matrix can provide some protection from ROS, but after solubilizing the mitochondria, this protection is lost and the SDH becomes more sensitive to sOMF.
TumCD↑, sOMF is highly effective at killing non-dividing GBM cell cultures,
Casp3↑, caspase-3 activation 1 h after sOMF
Casp7↑, rapid activation of caspase-3/7
MPT↑, OMF-treated cell that causes near simultaneous MPT, release of cytochrome c and other apoptosis-inducing factors, resulting in caspase-3/7 activation in these GBM cells.
Cyt‑c↑,
selectivity↑, differential sensitivity to sOMF of cancer cells over ‘normal’ cells becomes apparent. rapid increase in the reactive oxygen species (ROS) in the mitochondria to cytotoxic levels only in cancer cells, and not in normal human cortical neurons
GSH/GSSG↓, increasing GSSG/GSH ratio


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 21

Results for Effect on Cancer/Diseased Cells:
Akt↓,1,   angioG↓,3,   AntiCan↑,1,   Apoptosis↑,5,   Bak↑,1,   BAX↑,1,   Bcl-2↓,1,   Ca+2↓,1,   Ca+2↑,5,   Ca+2↝,1,   i-Ca+2↑,1,   Casp3↑,3,   Casp7↑,1,   Casp9↑,1,   Catalase↓,1,   chemoP↑,1,   ChemoSen↑,3,   Cyt‑c↑,2,   DNAdam↑,3,   Dose↝,1,   ECAR↓,1,   eff↓,4,   eff↑,6,   eff↝,4,   ER Stress↑,1,   F-actin↓,1,   Glycolysis↓,1,   Glycolysis∅,1,   GSH↓,1,   GSH/GSSG↓,2,   H2O2↑,2,   mt-H2O2↑,1,   HSP70/HSPA5↑,1,   lactateProd↑,1,   LIF↑,1,   mitResp↓,1,   MMP?,1,   MMP↓,5,   MMP2↑,1,   MPT↑,2,   mtDam↑,1,   mTOR↓,1,   OCR↓,1,   OCR↑,1,   OS↑,4,   OXPHOS↑,1,   PGC-1α↑,1,   i-pH↑,1,   PKM2↓,1,   RadioS↑,2,   Rho↓,1,   ROS↑,13,   ROS↝,1,   mt-ROS↑,1,   RPM↑,1,   SDH↓,1,   selectivity↑,20,   Slug↓,1,   p‑SMAD2↓,1,   p‑SMAD3↓,1,   SOD2↑,1,   p‑STAT3↑,1,   TCA?,1,   TGF-β↓,1,   Thiols↓,1,   TRPV1↑,1,   TumCD↑,3,   TumCG↓,4,   TumCI↓,2,   TumCMig↓,2,   TumCP↓,4,   TumVol↓,3,   Twist↓,1,   VEGF↓,1,   Vim↓,1,   β-catenin/ZEB1↓,1,   γH2AX↑,1,  
Total Targets: 77

Results for Effect on Normal Cells:
Akt↓,1,   angioG↑,1,   antiOx↑,1,   Ca+2↓,2,   Ca+2↑,1,   Ca+2∅,1,   i-Ca+2↓,1,   FGF↑,1,   HGF/c-Met↑,1,   IL1↑,1,   Inflam↓,2,   memory↑,1,   MMPs↑,1,   mTOR↓,1,   NF-kB↓,1,   PDGF↑,1,   ROS∅,1,   selectivity↑,2,   TNF-α↓,1,   TNF-α↑,1,   toxicity↓,2,   toxicity∅,4,   VEGF↑,1,  
Total Targets: 23

Scientific Paper Hit Count for: selectivity, selectivity
21 Magnetic Fields
6 Magnetic Field Rotating
1 Capsaicin
Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:172  Target#:1110  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

Home Page