toxicity Cancer Research Results

toxicity, toxicity: Click to Expand ⟱
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Type:
Toxicity
Scientific Papers found: Click to Expand⟱
1602- Cu,    A simultaneously GSH-depleted bimetallic Cu(ii) complex for enhanced chemodynamic cancer therapy†
- in-vitro, BC, MCF-7 - in-vitro, BC, 4T1 - in-vitro, Lung, A549 - in-vitro, Liver, HepG2
eff↑, enhanced chemodynamic cancer therapy
GSH↓, glutathione (GSH) depletion properties
H2O2↑, overexpressed H2O2
ROS↑, highly cytotoxic hydroxyl radicals (˙OH) that kill cancer cells
*BioAv↑, complex is quickly taken up by cancer cells and distributed in multiple organelles including mitochondria and the nucleus
selectivity↑, toxicity toward normal cells is significantly lower than that toward cancer cells due to the limited expression of H2O2
TumCCA↑, arrest the cell cycle of the G0/G1 phase
Apoptosis↑, inducing apoptosis rather than necrosis
Fenton↑, Cu+-involved reaction can occur with a highest reaction rate (1x10E4 M-1 s-1) in weakly acidic, which is about 160-fold increase over that of Fe2+
*toxicity?, C50 value of CuL-Cuphen to normal cells COS-7 was about 6.3uM.

6260- Cyste,    A novel sustained‐release cysteamine bitartrate formulation for the treatment of cystinosis: Pharmacokinetics and safety in healthy male volunteers
- Trial, Nor, NA
*toxicity?, In conclusion, a single dose of 600 mg PO‐001 was well tolerated with no findings of clinical concern

6288- DL,    From Citrus to Clinic: Limonene’s Journey Through Preclinical Research, Clinical Trials, and Formulation Innovations
- Review, Var, NA - Review, AD, NA
other↑, Limonene is an unparalleled terpenoid with numerous therapeutic benefits.
DDS↑, Incorporating it into sophisticated drug delivery systems and medical devices, together with personalised medicine strategies, signifies notable progress in its therapeutic use.
*antiOx↑, graohical abstract
*Inflam↓,
*AntiDiabetic↑,
*neuroP↑,
*Imm↑,
*Wound Healing↑,
*other↑, Limonene can act as a solvent for cholesterol and has, therefore, been used curatively to dissolve gallstones.
*BioAv↑, orally administered D-limonene shows complete absorption from the GI tract of both animals and humans.9
*ROS↓, thereby preventing the further generation of reactive oxygen species (ROS), as depicted in Figure 2
*SOD↑, D-limonene restored the activities of antioxidant enzymes, such as SOD, CAT, GP, and GSH level, further resulting in the reduction of oxidative stress by preventing DNA damage and protein denaturation. T
*Catalase↑,
*GSH↑,
*DNAdam↓,
*AntiDiabetic↑, D-limonene is found to reduce oxidative stress and induce the potentiation of beta cells in the pancreas, thus showing beneficial effects in diabetes mellitus
Casp3↑, D-limonene activates caspases 3 and 9
Casp9↑,
BAX↑, increases the expression of BAX protein, and decreases BCL2 protein expression,
Bcl-2↓,
*AChE↓, Limonene inhibited AChE and BChE activities by 10% and 12%, respectively.
*BChE↓,
*Aβ↓, Limonene decreased Aβ42-induced neuronal cell death and reduced ROS levels, adversely affecting extracellular signal-regulated kinase (ERK) phosphorylation
*ROS↓,
*toxicity?, D-limonene shows low toxicity effects and has not shown much affirmation in animal studies. Some studies have reported that they are non-carcinogenic in humans and do not show much toxicity, even after several years, when administered at low doses.

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↑, Ding et al., 8 it was demonstrated that 24‐h exposure to 60 Hz, 5 mT ELF‐EMF could potentiate apoptosis induced by H2O2 in HL‐60 leukaemia cell lines.
H2O2↑,
ROS↑, One of the main mechanisms proposed for defining anticancer effects of ELF‐EMF is induction of apoptosis through upregulation of reactive oxygen species (ROS) which has also been confirmed by different experimental studies.
eff↑, intermittent 100 Hz, 0.7 mT EMF significantly enhanced rate of apoptosis in human hepatoma cell lines pretreated with low‐dose X‐ray radiation.
eff↑, 50 Hz, 45 ± 5 mT pulsed EMF, significantly potentiated rate of apoptosis induced by cyclophosphamide and colchicine
Ca+2↑, Over the past few years, lots of data have shown that ELF‐EMF exposure regulates intracellular Ca2+ level
MAPK↑, Mitogen‐activated protein kinase (MAPK) cascades are among the other important signalling cascades which are stimulated upon exposure to ELF‐EMF in several types of examined cells
*Catalase↑, ELF‐EMF exposure can upregulate expression of different antioxidant target genes including CAT, SOD1, SOD2, GPx1 and GPx4.
*SOD1↑,
*GPx1↑,
*GPx4↑,
*NRF2↑, Activation and upregulation of Nrf2 expression, the master redox‐sensing transcription factor may be the most prominent example in this regard which has been confirmed in a Huntington's disease‐like rat model.
TumAuto↑, Activation of autophagy, ER stress, heat‐shock response and sirtuin 3 expression are among the other identified cellular stress responses to ELF‐EMF exposure
ER Stress↑,
HSPs↑,
SIRT3↑,
ChemoSen↑, Contrarily, when chemotherapy and ELF‐EMF exposure are performed simultaneously, this increase in ROS levels potentiates the oxidative stress induced by chemotherapeutic agents
UPR↑, In consequence of ER stress, cells begin to initiate UPR to counteract stressful condition.
other↑, Since the only proven effects of ELF‐EMF exposure on cells are cellular adaptive responses, ROS overproduction and intracellular calcium overload
PI3K↓, figure 3
JNK↑,
p38↑,
eff↓, ontrarily, when cells are exposed to ELF‐EMF, a new source of ROS production is introduced in cells which can at least partially reverse anticancer effects observed with cell's treatment with melatonin.
*toxicity?, More importantly, ELF‐EMF exposure to normal cells in most cases has shown to be safe and un‐harmful.

3296- SIL,    Silibinin induces oral cancer cell apoptosis and reactive oxygen species generation by activating the JNK/c-Jun pathway
- in-vitro, Oral, Ca9-22 - in-vivo, Oral, YD10B
TumCP↓, Silibinin effectively suppressed YD10B and Ca9-22 cell proliferation and colony formation in a dose-dependent manner.
TumCCA↑, Moreover, it induced cell cycle arrest in the G0/G1 phase, apoptosis, and ROS generation in these cells.
ROS↑,
SOD1↓, silibinin downregulated SOD1 and SOD2 and triggered the JNK/c-Jun pathway in oral cancer cells.
SOD2↓,
*JNK↑, inducing apoptosis, G0/G1 arrest, ROS generation, and activation of the JNK/c-Jun pathway.
toxicity?, Silibinin significantly inhibited xenograft tumor growth in nude mice, with no obvious toxicity.
TumCMig↓, Silibinin inhibits oral cancer cell migration and invasion
TumCI↓,
N-cadherin↓, silibinin downregulated N-cadherin and vimentin expression and upregulated E-cadherin expression in YD10B and Ca9-22 cells
Vim↓,
E-cadherin↑,
EMT↓, Together, these results indicate that silibinin inhibits the migration and invasion of oral cancer cells by suppressing the EMT.
P53↑, silibinin significantly induced the expression of p53, cleaved caspase-3, cleaved PARP, and Bax, and downregulated the expression of the anti-apoptotic marker protein Bcl-2
cl‑Casp3↑,
cl‑PARP↑,
BAX↑,
Bcl-2↓,
SOD↓, silibinin inhibits SOD expression, induces ROS production, and activates the JNK/c-Jun pathway in oral cancer cells.


Showing Research Papers: 1 to 5 of 5

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Fenton↑, 1,   GSH↓, 1,   H2O2↑, 2,   ROS↑, 3,   SIRT3↑, 1,   SOD↓, 1,   SOD1↓, 1,   SOD2↓, 1,  

Cell Death ⓘ

Apoptosis↑, 2,   BAX↑, 2,   Bcl-2↓, 2,   Casp3↑, 1,   cl‑Casp3↑, 1,   Casp9↑, 1,   JNK↑, 1,   MAPK↑, 1,   p38↑, 1,  

Transcription & Epigenetics ⓘ

other↑, 2,  

Protein Folding & ER Stress ⓘ

ER Stress↑, 1,   HSPs↑, 1,   UPR↑, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 1,  

DNA Damage & Repair ⓘ

P53↑, 1,   cl‑PARP↑, 1,  

Cell Cycle & Senescence ⓘ

TumCCA↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

EMT↓, 1,   PI3K↓, 1,  

Migration ⓘ

Ca+2↑, 1,   E-cadherin↑, 1,   N-cadherin↓, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 1,   Vim↓, 1,  

Drug Metabolism & Resistance ⓘ

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

Functional Outcomes ⓘ

toxicity?, 1,  
Total Targets: 40

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Catalase↑, 2,   GPx1↑, 1,   GPx4↑, 1,   GSH↑, 1,   NRF2↑, 1,   ROS↓, 2,   SOD↑, 1,   SOD1↑, 1,  

Cell Death ⓘ

JNK↑, 1,  

Transcription & Epigenetics ⓘ

other↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↓, 1,  

Immune & Inflammatory Signaling ⓘ

Imm↑, 1,   Inflam↓, 1,  

Synaptic & Neurotransmission ⓘ

AChE↓, 1,   BChE↓, 1,  

Protein Aggregation ⓘ

Aβ↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 2,  

Functional Outcomes ⓘ

AntiDiabetic↑, 2,   neuroP↑, 1,   toxicity?, 4,   Wound Healing↑, 1,  
Total Targets: 22

Scientific Paper Hit Count for: toxicity, toxicity
1 Copper and Cu NanoParticles
1 Cysteamine
1 D-limonene
1 Magnetic Fields
1 Silymarin (Milk Thistle) silibinin
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

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