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Toxicity

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4598-

AgNPs,

In vivo human time-exposure study of orally dosed commercial silver nanoparticles

in-vivo,

Nor,

62 Human voluneers

*toxicity∅, concluding no detectable toxicity
*Dose↝, 10 ppm oral silver particle dosing [36 subjects] and 32 ppm oral silver particle dosing [24 subjects]). 100 μg/day for 10 ppm, and 480 μg/day for 32 ppm silver
*Dose↝, corresponding to ionic silver comprising some 84.3% of the total silver content in the product administered orally to patients.
*BioAv↝, Peak serum silver concentration was detected in 42% of subjects in the 14-day 10 ppm dosing showing a mean of 1.6±0.4 mcg/L
*BioAv↝, The 32 ppm dose mean concentration was detected in 92% of subjects at 6.8±4.5 mcg/L
*H2O2∅, No statistically significant change in markers of hydrogen peroxide production or peroxiredoxin protein expression were detected.
*IL8∅, Analysis of IL-8, IL-1α, IL-1β, MCP1 and NQO1 also showed no statistical difference between the active silver and placebo solutions.
*IL1α∅,
*IL1β∅,
*MCP1∅,
*NQO1∅,
*BioAv↓, miniscule (<1%) amounts of 10-nm gold nanoparticles permeate across the gut to enter systemic vascular circulation from the intestine in rodents.51 We assert that silver metallic particle absorption is similar

2000-

AL,

Exploring the ROS-mediated anti-cancer potential in human triple-negative breast cancer by garlic bulb extract: A source of therapeutically active compounds

in-vitro,

BC,

MDA-MB-231

5–20 mg/mL

13.69 mg/mL

in-vitro,

BC,

MCF-7

5–20 mg/mL5–20 mg/mL

15.35 mg/mL

in-vitro,

Nor,

selectivity↑, The inhibitory effect of ASEE was more pronounced in MDA-MB-231 cells than in MCF-7 cells, however, no substantial cytotoxicity was seen in normal Vero cells.
TumCG?,
*toxicity∅, no substantial cytotoxicity was seen in normal Vero cells
ROS↑, TNBC cells treated with high concentrations of ASEE were found in the late apoptotic stage and exhibited an increase in ROS level and a reduction in MMP
MMP↓,
TumCCA↑, increased the percentage of cells in the G2/M phase
P53↑, ASEE upregulated the p53 and Bax proteins while downregulated the Bcl-2, p-Akt, and p-p38 proteins.
Bcl-2↓,
p‑Akt↓,
p‑p38↓,
*ROS∅, Vero normal cells did not display the unusual morphological alteration and reduction in cell viability. ROS production revealed a 1.21 % ROS level only in control cells that is typically seen in healthy cells.

234-

AL,

Allicin Induces Anti-human Liver Cancer Cells through the p53 Gene Modulating Apoptosis and Autophagy

in-vitro,

HCC,

Hep3B

 0, 15, 20, 25, 35, 40 and 50 Î¼M of allicin for 24 h

 35 uM @24h

ROS↑, increased the production of ROS levels at 1, 3, 6 h. I
*toxicity∅, In other study, allicin treatment did not increase the leakage of lactate-dehydrogenase (LDH) of primary rat hepatocytes until 1 mM allicin treated with rat hepatocytes24. For this reason, allicin could be inferred as safe to normal liver cells
MMP↓, Allicin decreased mitochondrial membrane potential
BAX↑,
Bcl-2↓,
AIF↑,
Casp3↑, protein expression levels of caspase-3, -8, -9 increased after allicin treatment
Casp8↑,
Casp9↑,
eff↓, Allicin significantly induced ROS overproduction, whereas NAC pretreatment decreased the ROS induction by allicin exposure in Hep 3B cells
γH2AX↑, significant increase in the expression of γ-H2AX was observed at the initial stages (3, 6 h), but not at the later stages of 12, 24, 48 h
selectivity↑, data suggested that allicin induced apoptosis in p53-deficiency human liver carcinoma cells but caused autophagy in p53-normal function human liver carcinoma cells.
DNA-PK↑, increases production of ROS, triggers DNA damage

3546-

ALA,

Cognitive and Mood Effect of Alpha-Lipoic Acid Supplementation in a Nonclinical Elder Sample: An Open-Label Pilot Study

Study,

AD,

fifteen elder patients (mean age: 84.5 ± 5.77) received ALA at a daily dose of 600 mg/day for 12 weeks.

*antiOx↑, (ALA), a known antioxidant compound abundant in vegetables and animal tissues, in reducing oxidative stress in the aging brain and preventing cognitive decline.
*ROS↓,
*cognitive∅, no statistically significant effects either on cognitive function, executive function, or mood were found
*lipid-P↓, ALA has been shown to reduce lipid peroxidation and increase the activity of antioxidant molecules in different areas of the brain of experimental animals
*memory↑, ALA has been suggested to improve memory by increasing the activity of choline acetyltransferase (ChAT)
*ChAT↑,
*Acetyl-CoA↑, a crucial step in the biosynthesis of acetylcholine, in the hippocampi of treated rats
*Aβ↓, ALA administration can inhibit the formation of beta-amyloid fibrils and their expansion, thus exerting a direct effect on a known mechanism involved in neurodegenerative diseases
*BioAv↑, ALA is abundantly present in vegetables and animal tissues [17], is promptly bioavailable, and has no known toxic effects on animals and human subjects
*BBB↑, ALA has been demonstrated to successfully cross the blood–brain barrier in animal models
*toxicity∅, and no collateral effects have been observed at the oral daily doses currently employed as supplements (from 50 to 2400 mg/day)

4759-

antiOx,

Chemo,

Potential Contributions of Antioxidants to Cancer Therapy: Immunomodulation and Radiosensitization

Review,

Var,

TumCD↑, curcumin has been shown to modulate immunoediting processes including resurrecting immune surveillance mechanisms to help eradicate cancer cells
TumCG↓, studies by Lee-Chang et al34 have shown that administration of resveratrol, a dietary polyphenol compound possessing antioxidant properties at low doses that are nontoxic to immune cells, inhibits lung metastasis of breast cancer tumor.
ROS⇅, Of importance, resveratrol can exert both antioxidant and pro-oxidant properties depending on its concentration and cell types used
eff↑, Wang et al36 have demonstrated that a combination of fish oil and selenium that possesses anti-inflammatory and antioxidant activities exerted synergistic effects in suppressing lung tumor growth mediated via decreasing the population of splenic Treg
RadioS↑, Several nutritional cancer chemopreventive compounds having antioxidant properties have been documented to potentiate radiation therapy–induced cytotoxic effects on cancer cells while reducing its toxicity on normal surrounding tissues.77-86
TumCG↓, soy isoflavone component genistein on prostate cancer demonstrated that both soy and genistein inhibited the growth of in vitro human PC-3 prostate cancer cells and in vivo orthotopic PC-3 tumors
OS↑, While a statistically significant improved survival rate either at 1 year or 5 years was associated with melatonin supplementation
toxicity∅, 9 RCTs reported no differences in the toxicities by antioxidants supplementation
toxicity↑, and 1 RCT with vitamin A reported increased toxicity.

1549-

Api,

Chemo,

Chemoprotective and chemosensitizing effects of apigenin on cancer therapy

Review,

NA,

ChemoSideEff↓, combination therapies with apigenin could suppress the unwanted toxicity of chemotherapeutic agents
*toxicity∅, apigenin resulted in no mortality or signs of toxicity in mice/rats at oral doses up to 5000 mg/kg
ChemoSen↑, based on its chemosensitizing effect
eff↑, 5-FU and apigenin at 90 μM and 10 μM concentrations, respectively. This co-therapy led to a significant reduction in ErbB2 and protein kinase B (AKT) expression and AKT phosphorylation as compared to monotherapy
eff↑, molecular analysis of the renal cells demonstrates that pre-treatment by apigenin significantly reduced cisplatin-induced renal injury by anti-oxidant and anti-inflammatory effects.
eff↑, They suggested that metformin and apigenin synergistically inhibited mitochondrial membrane potency and this effect was attributed to a notable increase in ROS levels in cancer cells.

1562-

Api,

Apigenin protects human melanocytes against oxidative damage by activation of the Nrf2 pathway

in-vitro,

Vit,

*SOD↑,
*Catalase↑,
*GPx↑, GSH-Px
*MDA↓,
*NRF2↑, Nrf2 transcription factor, an important regulator oxidative stress and its downstream target genes, was significantly increased by apigenin treatment
*toxicity∅, Apigenin’s non-toxicity

1558-

Api,

Preparation, characterization and antitumor activity evaluation of apigenin nanoparticles by the liquid antisolvent precipitation technique

in-vitro,

Liver,

HepG2

BioAv↑, oral bioavailability of apigenin nanoparticles was about 4.96 times higher than that of the raw apigenin
*toxicity∅, apigenin nanoparticles had no toxic effect on the organs of rats.
eff↑, higher inhibition to HepG2 cells by lower IC50 than that of raw apigenin. In addition, The IC50 values of apigenin nanoparticles and raw apigenin were separately 89.33 and 216.84 μg/mL

5422-

ASTX,

Improved intestinal absorption and oral bioavailability of astaxanthin using poly (ethylene glycol)-graft-chitosan nanoparticles: preparation, in vitro evaluation, and pharmacokinetics in rats

in-vivo,

Nor,

*antiOx↑, Astaxanthin (ASTA) is a kind of food-derived active ingredient (FDAI) with antioxidant and antidiabetic functions.
*AntiDiabetic↑,
*toxicity∅, It is nontoxic but its poor solubility and low bioavailability hinder its application in the food industry.
*BioAv↓,
*BioAv↑, n this study, a novel carrier, polyethylene glycol-grafted chitosan (PEG-g-CS) was applied to enhance the bioavailability of astaxanthin.

1533-

Ba,

Baicalein, as a Prooxidant, Triggers Mitochondrial Apoptosis in MCF-7 Human Breast Cancer Cells Through Mobilization of Intracellular Copper and Reactive Oxygen Species Generation

in-vitro,

BrCC,

MCF-7

85μM for 24 h

in-vitro,

Nor,

MCF10

557uM

tumCV↓,
i-ROS↑, enhancement the level of intracellular ROS exhibit pro-oxidant activity in the presence of copper ions
MMP↓,
Bcl-2↓,
BAX↑,
Cyt‑c↑, release of cytochrome C
Casp9↑,
Casp3↑,
eff↓, The pretreatment with NeoCu (I)-specific chelator) remarkably weakened these effects of baicalein exhibit pro-oxidant activity in the presence of copper ions
selectivity↑, baicalein presented little cytotoxicity to normal breast epithelial cells
*toxicity∅, baicalein presented little cytotoxicity to normal breast epithelial cells. explained by the undetectable levels of copper present in MCF-10A cells.
Apoptosis↑,
Fenton↑, results are in further support that the prooxidant action of baicalein involves the reduction of Cu (II) to Cu (I), and the consequent generation of hydroxyl radicals.

2618-

Ba,

Baicalein induces apoptosis by inhibiting the glutamine-mTOR metabolic pathway in lung cancer

in-vitro,

Lung,

H1299

12.5, 25, and 50 μM

in-vivo,

Lung,

A549

10, 20, and 40 μM

TumCG↓, Baicalein inhibited lung cancer xenograft tumor growth in vivo and suppressed proliferation and promoted apoptosis in lung cancer cells in vitro.
TumCP↓,
Apoptosis↑,
GLUT1↓, baicalein interacted with glutamine transporters as well as glutaminase and inhibited their activation
GLS↓,
mTOR↓, mTOR, an apoptosis-related protein and downstream target of glutamine metabolism, was also inhibited by baicalein treatment
*toxicity∅, baicalein treatment did not result in damage to the mouse organs, including the liver, heart, spleen, lung, or kidney
cl‑Casp9↓, baicalein dose-dependently suppressed the protein levels of Bax, cleaved caspase 9, and cleaved caspase 3 in H1299 and A549 cells
cl‑Casp3↓,
GSH↓, Meanwhile, the levels of glutathione (GSH), S-formylglutathione, and pyroglutamic acid in baicalein-treated A549 cells were downregulated when compared to that in control group
GlutMet↓, These findings indicate that baicalein inhibits cellular glutamine uptake, which is consistent with the findings of metabolomics studies.

5473-

BM,

Bacopa monnieri: Preclinical and Clinical Evidence of Neuroactive Effects, Safety of Use and the Search for Improved Bioavailability

in-vivo,

AD,

in-vivo,

Park,

*neuroP↑, results in reducing symptoms and protecting against neurodegeneration.
*toxicity∅, Bacopa monnieri has been found to be generally non-toxic, with no serious side effects reported.
*AChE↓, The neuroprotective effect of Bacopa monnieri was likely due to its ability to inhibit acetylcholinesterase activity rather than mitigating glutamate-induced toxicity.
*ROS↓, neurons treated with the extract exhibited lower levels of reactive oxygen species, suggesting a reduction in intracellular oxidative stress and an extension of neuronal lifespan.
*antiOx↑, The extract also demonstrated antioxidant properties and inhibited lipid peroxidation
*lipid-P↓,
*cognitive↑, on 72 mice, it was shown that supplementation with Bacopa monnieri (100 mg/kg for 180 days) significantly improved cognitive function.
*memory↑, 60 healthy, elderly volunteers taking 300 mg and 600 mg of Brahmi showed reduced acetylcholinesterase activity, which resulted in improved attention and memory.
*Dose↝, Ethanol extract was most commonly used in the studies. Doses are usually in the range of 300 to 600 mg daily.
*BioAv↓, Bacoside A is one of the main active compounds found in Bacopa monnieri. However, its water insolubility results in low bioavailability when administered orally.
*TumCCA↑, It has been shown to induce cell cycle arrest and apoptosis in colorectal cancer cell lines
*BBB↝, Studies were also conducted in which, similarly to the aforementioned approach, formulated solid lipid nanoparticles (SLNs) were used to facilitate the transport of the bacoside-rich extract across the blood–brain barrier.

2014-

CAP,

Role of Mitochondrial Electron Transport Chain Complexes in Capsaicin Mediated Oxidative Stress Leading to Apoptosis in Pancreatic Cancer Cells

in-vitro,

PC,

Bxpc-3

150uM

in-vitro,

Nor,

HPDE-6

150uM

normal pancreatic epithelial cells were resistant to the effects of capsaicin.

in-vivo,

PC,

AsPC-1

mice orally fed with 2.5 mg/kg capsaicin

mice, 2.5 mg/kg capsaicin was given to mice by oral gavage, which is 0.202 mg/kg when converted to human equivalent dose (HED) and equates to 13.2 mg dose of capsaicin for a 60 kg person

ROS↑, ROS was about 4–6 fold more as compared to control and as early as 1 h after capsaicin treatment in BxPC-3 and AsPC-1 cells
*ROS∅, but not in normal HPDE-6 cells
selectivity↑, only small ~1.2fold ROS increase in normal cell
compI↓, capsaicin inhibits about 2.5–9% and 5–20% of complex-I activity
compIII↓, and 8–75% of complex-III activity in BxPC-3 and AsPC-1 cells respectively
eff↑, which was attenuable by SOD, catalase and EUK-134.
selectivity↑, capsaicin treatment failed to inhibit complex-I or complex-III activities in normal HPDE-6 cells
ATP↓, ATP levels were drastically suppressed by capsaicin treatment in both BxPC-3 and AsPC-1 cells
Cyt‑c↑, release of cytochrome c and cleavage of both caspase-9 and caspase-3 due to disruption of mitochondrial membrane potential
Casp9↑,
Casp3↑,
MMP↓,
SOD↓, mice orally fed with 2.5 mg/kg capsaicin show decreased SOD activity and an increase in GSSG/GSH levels as compared to controls
GSH/GSSG↓, mice orally fed with 2.5 mg/kg capsaicin
Apoptosis↑, Capsaicin triggers apoptosis in pancreatic cancer cells but not in normal HPDE-6 cells
*toxicity∅, Capsaicin triggers apoptosis in pancreatic cancer cells but not in normal HPDE-6 cells
GSH↓, Taken together, our results suggest that depletion of GSH level and inhibition of SOD, catalase and GPx by capsaicin disturbs the cellular redox homeostasis resulting in increased oxidative stress.
Catalase↓,
GPx↓,
Dose↝, 13.2 mg dose of capsaicin for a 60 kg person

5889-

CAR,

Effect of carvacrol on pulmonary function tests, and total and differential white blood cell counts in healthy volunteers: A randomized clinical trial

Trial,

Nor,

*Dose↝, carvacrol (1 and 2 mg/kg/day) for 1 month.
*toxicity∅, The results of this study indicated that treatment of healthy individuals with 1 and 2 mg/kg carvacrol for 1 month has no negative effects on total and differential WBC counts nor PFT values.

3877-

Carno,

Carnosine, diabetes and Alzheimer's disease

Review,

AD,

*toxicity∅, arnosine, an almost nontoxic natural product, satisfies the criteria proposed by Maher and Schubert [1], that lead compounds should possess for eventual development of drugs to combat AD and T2D.
*antiOx↑, Carnosine is an antioxidant [9–11] and antiglycating agent that inhibits sugar-mediated protein crosslinking [12–14] and also chelates a number of metal ions (including copper and zinc)
IronCh↑,

3878-

Carno,

Safety and Efficacy Evaluation of Carnosine, An Endogenous Neuroprotective Agent for Ischemic Stroke

in-vivo,

Stroke,

*toxicity∅, carnosine did not exhibit any evidence of adverse effects or toxicity.
*antiOx↑, In primary neuronal cell cultures and ex vivo brain homogenates, carnosine exhibited robust anti-excitotoxic, antioxidant, and mitochondria protecting activity.
*neuroP↑, arnosine treatment exhibited significant cerebroprotection against histological and functional damage
*IronCh↑, Carnosine exhibits pleiotropic biological activities such as antioxidant, cytosolic buffering, heavy metal chelating and anti-excitotoxic activity.
*ROS↓, In both models, carnosine decreased reactive oxygen species generation, supporting its role as an antioxidant

1574-

Citrate,

Citrate Suppresses Tumor Growth in Multiple Models through Inhibition of Glycolysis, the Tricarboxylic Acid Cycle and the IGF-1R Pathway

in-vitro,

Lung,

A549

5,10,15mM

in-vitro,

Melanoma,

WM983B

in-vivo,

NA,

4 g/kg citrate twice a day for 4 week

mice. Plasma levels in chronically treated animals were approximately 3 mM

TumCG↓,
eff↑, additional benefit accrued in combination with cisplatin
T-Cell↑, significantly higher infiltrating T-cells
p‑IGF-1R↓, citrate inhibited IGF-1R phosphorylation
p‑Akt↓, inhibited AKT phosphorylation
PTEN↑, activated PTEN
p‑eIF2α↑, increased expression of p-eIF2a p-eIF2a was decreased when PTEN was depleted
OCR↓, citrate treatment of A549 cells dramatically reduced oxygen consumption
ROS↓, observed a decrease in ROS in A549
ECAR∅, acidification rate (ECAR) and found it to be unchanged
IL1↑, s (e.g. interleukin-1, tumor necrosis factor-alpha, etc) and anti-inflammatory cytokines (e.g. interleukin-10 and interleukin 1 receptor antagonist) are activated
TNF-α↑,
IL10↑,
IGF-1R↓, Citrate Inhibits IGF-1R Activation And Its Downstream Pathway
eIF2α↑, eIF2α activity was increased in A549 cells after citrate treatment
PTEN↑, PTEN was activated
TCA↓,
Glycolysis↓, citrate may inhibit tumor growth via inhibiting glycolysis and the TCA cycle and that this effect appears to be selective to tumor tissue.
selectivity↑, citrate may inhibit tumor growth via inhibiting glycolysis and the TCA cycle and that this effect appears to be selective to tumor tissue.
*toxicity∅, Chronic citrate treatment was non-toxic as evidenced by gross pathology in numerous organs (liver, lung, spleen and kidney)
Dose∅, corresponding to approximately 56 g of citrate in a 70 kg person

1603-

Cu,

BP,

SDT,

Glutathione Depletion-Induced ROS/NO Generation for Cascade Breast Cancer Therapy and Enhanced Anti-Tumor Immune Response

in-vitro,

BC,

4T1

in-vivo,

NA,

mice

GSH↓, Cu2O was incorporated into BP(black phosphorus) to exhaust the overexpressed intracellular GSH
Fenton↑, However, the Cu+-catalyzed Fenton reaction converts H2O2 into OH at a high reaction rate, even in a neutral environment (160 times than that of Fe2+)
ROS↑, BCL nanoparticles exhibited multifunctional characteristics for GSH depletion-induced ROS/NO generation,
NO↑,
sonoS↑, Numerous studies have confirmed that BP, as a sonosensitizer, can induce ROS generation in cancer therapy
eff↑, These results indicated that an acidic environment can effectively promote Cu release.
NO↑, massive NO production
*toxicity∅, Additionally, no significant body weight loss or apparent histological abnormalities of the major organs (heart, liver, spleen, lungs, and kidneys) were observed, indicating the negligible organ toxicity
eff?, In vivo studies demonstrated that BCL plus US treatment could significantly inhibit tumor growth

3574-

CUR,

The effect of curcumin (turmeric) on Alzheimer's disease: An overview

Review,

AD,

*antiOx↑, Curcumin as an antioxidant, anti-inflammatory and lipophilic action improves the cognitive functions in patients with AD
*Inflam↓,
*lipid-P↓,
*cognitive↑,
*memory↑, overall memory in patients with AD has improved.
*Aβ↓, curcumin may help the macrophages to clear the amyloid plaques found in Alzheimer's disease.
*COX2↓, Curcumin is found to inhibit cyclooxygenase (COX-2),
*ROS↓, The reduction of the release of ROS by stimulated neutrophils, inhibition of AP-1 and NF-Kappa B inhibit the activation of the pro-inflammatory cytokines TNF (tumor necrosis factor)-alpha and IL (interleukin)-1 beta
*AP-1↓,
*NF-kB↓,
*TNF-α↓,
*IL1β↓,
*SOD↑, It also increased the activity of superoxide dismutase, sodium-potassium ATPase that normally decreased with aging.
*GSH↑, followed by a significant elevation in oxidized glutathione content.
*HO-1↑, curcumin induces hemoxygenase activity.
*IronCh↑, curcumin effectively binds to copper, zinc and iron.
*BioAv↓, Curcumin has poor bioavailability. Because curcumin readily conjugated in the intestine and liver to form curcumin glucuronides.
*Half-Life↝, , serum curcumin concentrations peaked one to two hours after an oral dose
*Dose↝, Peak serum concentrations were 0.5, 0.6 and 1.8 micromoles/L at doses of 4, 6 and 8 g/day respectively.
*BBB↑, Curcumin crosses the blood brain barrier and is detected in CSF
*BioAv↑, Absorption appears to be better with food.
*toxicity∅, A phase 1 human trial with 25 subjects using up to 8000 mg of curcumin per day for three months found no toxicity from curcumin.
*eff↑, Co-supplementation with 20 mg of piperine (extracted from black pepper) significantly increase the bioavailablity of curcumin by 2000%

1864-

DCA,

MET,

Dichloroacetate Enhances Apoptotic Cell Death via Oxidative Damage and Attenuates Lactate Production in Metformin-Treated Breast Cancer Cells

in-vitro,

BC,

MCF-7

DCA (2.5 mM) and metformin (1 mM)

in-vitro,

BC,

T47D

in-vitro,

Nor,

MCF10

PDKs↓, Dichloroacetate (DCA) is a well-established drug used in the treatment of lactic acidosis which functions through inhibition of pyruvate dehydrogenase kinase (PDK) promoting mitochondrial metabolism
eff↑, DCA and metformin are used in combination, synergistic induction of apoptosis of breast cancer cells occurs.
ROS↑, Metformin-induced oxidative damage is enhanced by DCA through PDK1 inhibition which also diminishes metformin promoted lactate production.
PDK1↓,
lactateProd↓, also diminishes metformin promoted lactate production.
p‑PDH↑, DCA is an inhibitor of pyruvate dehydrogenase kinase (PDK) which phosphorylates pyruvate dehydrogenase (PDH), rendering it inactive
Dose∅, DCA (2.5 mM) and metformin (1 mM)
OCR↑, DCA treated cells had a significantly higher oxygen consumption rate compared to control cells.
DNA-PK↑,
γH2AX↑, phosphorylatoin of histone H2AX (p-H2AX), which is a useful surrogate marker of such DNA damage
cl‑PARP↑, large increase of cleaved PARP
selectivity↑, Importantly, we also show that this combination of drugs does not kill non-transformed breast epithelial cells MCF10A under the same conditions in which the drugs kill cancer cells.
*toxicity∅, does not kill non-transformed breast epithelial cells MCF10A under the same conditions in which the drugs kill cancer cells.

1873-

DCA,

Dual-targeting of aberrant glucose metabolism in glioblastoma

in-vitro,

GBM,

U87MG

in-vitro,

GBM,

U251

PDKs↓, dichloroacetate (DCA), a pyruvate dehydrogenase kinase inhibitor.
eff↑, By combining DCA with PENAO, the two drugs worked synergistically to inhibit cell proliferation (but had no significant effect on non-cancerous cells)
selectivity↑,
MMP↓, induced oxidative stress and depolarized mitochondrial membrane potential, which in turn activated mitochondria-mediated apoptosis
ROS↑,
Apoptosis↑,
Warburg↓, Dichloroacetate (DCA), a pyruvate dehydrogenase kinase (PDK) inhibitor that reverses the Warburg effect
eff↑, DCA has been demonstrated to sensitize cancer cells towards apoptosis and enhance the effects of several anti-cancer agents, including arsenic trioxide [20], cisplatin [22,23] and metformin [24].
Dose∅, IC50 values of DCA were at suprapharmacological millimolar level
toxicity∅, whilst the IC50 values of DCA for non-cancerous cells were not reached (DCA concentration in this study was tested up to 50 mM)

1868-

DCA,

MET,

Long-term stabilization of stage 4 colon cancer using sodium dichloroacetate therapy

Case Report,

NA,

eff↑, DCA therapy resulted in tumour stabilization of stage 4 colon cancer in a 57 years old female for a period of nearly 4 years, with no serious toxicity
toxicity∅,
MMP↓, In the initial 2007 paper by Bonnet et al[1], it was reported that DCA reduced mitochondrial membrane potential resulting in selective apoptosis in cancer cells.
Apoptosis↑,
selectivity↑,
pH↝, alteration of pH regulators V-ATPase and MCT1
Dose↝, The neuropathy risk with inclusion of natural neuroprotective agents was roughly 20% with 20-25 mg/kg per day dosing on a 2 wk on/1 wk off cycle.
Dose↝, 3 natural supplements were prescribed: Alpha lipoic acid (racemic) 500 mg i.v. with each DCA dose, oral R-alpha lipoic acid 150 mg 3 times a day, oral acetyl L-carnitine 500 mg 3 times a day, and oral benfotiamine 80 mg twice a day.
eff↑, Oral metformin was added to help sensitize the cancer to the chemotherapy, starting at 500 mg orally once a day with titration up to 500 mg 3 times a day

1889-

DCA,

A mitochondria-K+ channel axis is suppressed in cancer and its normalization promotes apoptosis and inhibits cancer growth

Review,

Var,

PDKs↓, Dichloroacetate (DCA) inhibits mitochondrial pyruvate dehydrogenase kinase (PDK)
Glycolysis↓, shifts metabolism from glycolysis to glucose oxidation
mt-H2O2↑, increases mitochondrial H2O2
Apoptosis↑, DCA induces apoptosis, decreases proliferation, and inhibits tumor growth, without apparent toxicity
TumCP↓,
TumCG↓,
toxicity∅,

1446-

Deg,

Efficacy and mechanism of action of Deguelin in suppressing metastasis of 4T1 cells

in-vitro,

BC,

4T1

250nM

cMET↓,
p‑ERK↓,
p‑Akt↓,
TumCMig↓,
TumCG↓, vivo
Weight∅, no difference in the body weight as well as liver and spleen weights between vehicle treated control and Deguelin treated animals indicating that Deguelin was nontoxic at the dose used
*toxicity∅, no difference in the body weight as well as liver and spleen weights between vehicle treated control and Deguelin treated animals indicating that Deguelin was nontoxic at the dose used
Hif1a↓, Deguelin inhibits both ERK and p-AKT pathway leading to reduced expression of HIF −1α.
TumMeta↓,

1849-

dietFMD,

The emerging role of fasting-mimicking diets in cancer treatment

Review,

Var,

TumCG↓, Accumulating evidence suggests that FMDs attenuate tumor growth by altering the energy metabolism of cancer cells
toxicity∅, FMD reduces risk factors and markers for aging, cardiovascular disease, diabetes, and cancer without serious adverse effects in healthy adults.
BG↓, dramatic downregulation of blood glucose
IGF-1↓, prolonged fasting downregulated IGF-1
mTOR↓, inhibits cellular mTOR activity.
M2 MC↓, In addition, alternate-day fasting inhibited colorectal cancer growth by suppressing adenosine-induced M2 macrophage polarization in the tumor microenvironment
eff↑, large prospective cohort study of breast cancer patients, a longer nightly fasting duration was associated with a decreased risk of breast cancer recurrence, so the FMD may also be beneficial after the eradication of the initial tumo
ChemoSen↑, Combining fasting cycles with chemotherapeutic agents markedly prevented the progression of subcutaneous breast cancer, melanoma, and glioma in mouse models
QoL↑, Fasting for 60 hours seemed to improve the patients' fatigue and quality of life during chemotherapy
RadioS↑, In response to stress, cancer cells engage antioxidant and DNA repair mechanisms in an energy-demanding manner, facilitating cancer cell survival. Thus, restriction of the energy supply would improve the antitumor activity of radiotherapy.
selectivity↑, Recently, short-term starvation was shown to increase the DNA damage induced by a single exposure to high-dose radiation in metastatic cancer cell lines, whereas healthy cells were not affected by starvation medium

1853-

dietFMD,

Impact of Fasting on Patients With Cancer: An Integrative Review

Review,

Var,

*toxicity∅, Data suggest overall good compliance, no malnutrition, minimal side effects. No significant changes were identified to suggest increased harm.
QoL∅, unchanged quality of life (QOL),
eff↑, improved endocrine parameters
eff↝, mixed results for cancer outcomes
ChemoSideEff↓, decreasing chemotherapy-related side effects
TumCG↓, limiting tumor growth
Dose↑, When fasting is used as an adjunct to chemotherapy, a minimum fasting period of at least 48 hours is currently recommended for nutritional interventions in order to achieve a measurable metabolic response at the cellular level
toxicity↝, The increased risk for poor outcomes associated with malnutrition, weight loss, and cachexia poses an obvious safety concern for patients with cancer who participate in calorie-restricted fasting
eff↑, short-term fasting involving water-only or limited daily calorie consumption for less than a week has the potential to achieve positive metabolic changes while avoiding malnutrition and significant weight loss
IGF-1↑, statistically significant decrease in IGF-1 among participants compliant with fasting compared with regular diet during the middle of therapy
*OXPHOS↑, Healthy cells also use mitochondrial oxidative phosphorylation for metabolism while cancer cells use aerobic glycolysis, also known as the Warburg effect
BG↓, statistically significant decrease in glucose among participants compliant with fasting compared with controls
Insulin↓, statistically significant decrease in insulin among participants compliant with fasting compared with regular diet before the first cycle of chemotherapy (p = .001), as well as during the middle of therapy
RadioS↑, A complete or partial radiographic response was also noted more often among fasting participants compared with normal diet participants

1810-

dietKeto,

Oxy,

The Ketogenic Diet and Hyperbaric Oxygen Therapy Prolong Survival in Mice with Systemic Metastatic Cancer

in-vivo,

Var,

mice

BG↓, KD alone significantly decreased blood glucose, slowed tumor growth, and increased mean survival time by 56.7% in mice with systemic metastatic cancer.
TumCG↓,
OS↑,
eff↑, While HBO2T alone did not influence cancer progression, combining the KD with HBO2T elicited a significant decrease in blood glucose, tumor growth rate, and 77.9% increase in mean survival time compared to controls.
Dose∅, Mice undergoing HBO2T received 100% O2 for 90 minutes at 1.5 ATM gauge (2.5 ATM absolute) three times per week (M, W, F) in a hyperbaric chamber (Model 1300B, Sechrist Industries, Anaheim, CA).
KeyT↑, only the KD+HBO2T animals showed significantly increased ketones compared to controls
eff↑, we hypothesized that combining these non-toxic treatments would provide a powerful, synergistic anti-cancer effect.
cachexia↓, While low carbohydrate or ketogenic diets promote weight loss in overweight individuals, they are also known to spare muscle wasting during conditions of energy restriction and starvation
ChemoSen↑, KD improves quality of life and enhances the efficacy of chemotherapy treatment in the clinic
*ROS↓, ketone body metabolism protects cells from oxidative damage by decreasing ROS production. cancer cells are unable to effectively metabolize ketone bodies; we do not expect that ketones would confer the same protective effects onto the cancer cells
ROS↑, HBO2T increases ROS production within the cell which can lead to membrane lipid peroxidation and cell death
lipid-P↑,
selectivity↑, KD weakens cancer cells by glucose restriction and the inherent anti-cancer effects of ketone bodies while simultaneously conferring a protective advantage to the healthy tissue capable of ketone metabolism.
toxicity∅, HBO2T should be considered a safe treatment for patients with varying malignancies and that there is no convincing evidence its use promotes cancer progression or recurrence

1607-

EA,

Exploring the Potential of Ellagic Acid in Gastrointestinal Cancer Prevention: Recent Advances and Future Directions

Review,

GC,

STAT3↓, EA inhibits STAT3 signaling
TumCP↓, EA inhibits cell proliferation, induces apoptosis
Apoptosis↑,
NF-kB↓, inhibiting nuclear factor-kappa B
EMT↓, suppressing epithelial–mesenchymal transition
RadioS↑, In liver cancer, EA exhibits radio-sensitizing effects
antiOx↑, As a potential antioxidant agent,
COX1↓, EA suppresses the expression of several factors, including COX1, COX2, c-myc, snail, and twist1
COX2↓,
cMyc↓,
Snail↓,
Twist↓,
MMP2↓, significantly decreased MMP-2 and MMP-9 expression and activity.
P90RSK↓,
CDK8↓, downregulate CDK8 expression and activity
PI3K↓, inactivating PI3K/Akt signaling
Akt↓,
TumCCA↑, promote cell cycle arrest
Casp8↑, ctivating caspase-8, and lowering proliferating cell nuclear antigen (PCNA) expression,
PCNA↓,
TGF-β↓,
Shh↓, suppression of the Akt, Shh, and Notch pathways, EA can prevent the growth, angiogenesis, and metastasis of pancreatic cancer
NOTCH↓,
IL6↓,
ALAT↓, decreasing liver injury biomarkers such as alanine transaminase (ALT), alkaline phosphatase (ALP), and aspartate aminotransferase (AST)
ALP↓,
AST↓,
VEGF↓,
P21↑,
*toxicity∅, no toxicity was found for a 50% effective dose by the intraperitoneal route inferior to 1 mg/kg/day
*Inflam↓, ncluding anti-inflammatory [10], anti-oxidant [11], anti-allergic [12], and anti-mutagenic [13] properties, as well as potential health advantages like gastroprotective [14], cardioprotective [15], neuroprotective [16, 17], and hepatoprotective [18,
*cardioP↑,
*neuroP↑,
*hepatoP↑,
ROS↑, Exposure to EAs induced apoptosis, accelerated cell cycle arrest, and elevated the generation of reactive oxygen intermediates [59].
*NRF2↓, As a potential antioxidant agent, it scavenges reactive oxygen species (ROS), and by upregulating of Nrf2,
*GSH↑, Moreover, EA increases reduced glutathione (GSH), which is critical for cellular defense against oxidative stress and liver damage,

1613-

EA,

Ellagitannins in Cancer Chemoprevention and Therapy

Review,

Var,

ROS↑, pomegranate ET inhibit pro-inflammatory pathways including, but not limited to, the NF-κB pathway, whose activation leads to immune reactions, inflammation, and the transcription of genes involved in cell survival, such as Bclx and inhibitors of apop
angioG↓, ET to inhibit angiogenesis
ChemoSen↑, ET could also be utilized to increase the sensitivity of tumor cells to standard chemotherapeutic drugs
BAX↑, induction of pro-apoptotic mediators (Bax and Bak), downregulation of Bcl-2 and Bcl-XL, and reduced expression of cyclin-dependent kinases 2, 4, 6, and cyclins D1, D2, and E
Bak↑,
Bcl-2↓,
Bcl-xL↓,
CDK2↓,
CDK4↓,
CDK6↓,
cycD1/CCND1↓,
cycE1↓,
TumCG↓, reduced LNCaP prostate cancer xenograft size, tumor vessel density, VEGF peptide levels and HIF-α expression after four weeks of treatment in severe combined immunodeficient mice
VEGF↓,
Hif1a↓,
eff↑, Oenothein B, a macrocyclic ET, and quercetin-3-O-glucuronide from Epilobium sp. herbs—used in traditional medicine to treat benign prostatic hyperplasia and prostatic adenoma—have been proven to strongly inhibit the proliferation of human prostate ca
COX2↓, pomegranate ET (i.e., punicalagin and ellagic acid) have been shown to suppress cyclooxygenase-2 (COX-2) protein expression in human colon cancer (HT-29) cells
TumCCA↑, pomegranate ET and their metabolites, i.e., urolithins A and C, inhibit HT-29 cells proliferation via G0/G1 and G2/M arrest
selectivity↑, interestingly, normal human breast epithelial cells (MCF-10A) were far less sensitive to the inhibitory effect of polyphenol-rich fractions.
Wnt/(β-catenin)↓, suppression of Wnt/β-catenin
*toxicity∅, LD50 of a standardized pomegranate fruit extract containing 30% punicalagin in Wistar rats was >5 g/kg b.w.,

1618-

EA,

A comprehensive review on Ellagic acid in breast cancer treatment: From cellular effects to molecular mechanisms of action

Review,

BC,

TumCCA↑, suppresses the growth of BC cells by arresting the cell cycle in the G0/G1 phase,
TumCMig↓, suppresses migration, invasion, and metastatic
TumCI↓,
TumMeta↓,
Apoptosis↑, stimulates apoptosis in MCF-7 cells via TGF-β/Smad3 signaling axis
TGF-β↓,
SMAD3↓,
CDK6↓, inhibits CDK6 that is important in cell cycle regulation,
PI3K↓, inhibits the PI3K/AKT pathway
Akt↓,
angioG↓,
VEGFR2↓, reduces VEGFR-2 tyrosine kinase activity
MAPK↓,
NEDD9↓, downregulated protein 9 (NEDD-9)
NF-kB↓, EA suppressed NF-κB precursor protein p105
eff↑, They showed that the encapsulation of EA in biodegradable polymeric nanoparticles would improve the bioavailability after oral administration and also enhance the anticancer properties
eff↑, Chitosan nanoparticles and EA with high anticancer efficacy could be a suitable therapeutic strategy
RadioS↑, showed that the synergistic effect of EA combined with radiotherapy/chemotherapy resulted in increased DNA damage and apoptosis as well as decreased levels of MGMT expression
ChemoSen↑,
DNAdam↑,
eff↑, combination of Paclitaxel and EA has shown promise in inhibiting tumor growth and metastasis in experimental BC models.
*toxicity∅, 630 mg/kg is the LD50 of EA in the rat population.
*toxicity∅, no-observed adverse effect level of EA is 2000 mg/kg body weight

3208-

EGCG,

Induction of Endoplasmic Reticulum Stress Pathway by Green Tea Epigallocatechin-3-Gallate (EGCG) in Colorectal Cancer Cells: Activation of PERK/p-eIF2α/ATF4 and IRE1α

in-vitro,

Colon,

HT29

in-vitro,

Nor,

3T3

TumCD↓, EGCG treatment was toxic to the HT-29 cell line
ER Stress↑, EGCG induced ER stress in HT-29 by upregulating immunoglobulin-binding (BiP), PKR-like endoplasmic reticulum kinase (PERK), phosphorylation of eukaryotic initiation factor 2 alpha subunit (eIF2α), activating transcription 4 (ATF4), and IRE1α
GRP78/BiP↑,
PERK↑,
eIF2α↑,
ATF4↑,
IRE1↑,
Apoptosis↑, Apoptosis was induced in HT-29 cells after the EGCG treatment, as shown by the Caspase 3/7 activity.
Casp3↑,
Casp7↑,
Wnt↓, (CRC) via suppression of the Wnt/β-catenin pathway
β-catenin/ZEB1↓,
*toxicity∅, This embryonic fibroblast cell line (3T3) has shown that the EGCG was not toxic to normal healthy cells, given the treatment at any concentration even at the highest concentration of EGCG (1000 μM).
UPR↑, ER stress is induced by EGCG and activates UPR proteins

1514-

EGCG,

Preferential inhibition by (-)-epigallocatechin-3-gallate of the cell surface NADH oxidase and growth of transformed cells in culture

in-vitro,

Cerv,

HeLa

1-50uM

in-vitro,

Nor,

MCF10

selectivity↑, EGCg preferentially inhibited growth of HeLa and mammary adenocarcinoma cells compared with growth of mammary epithelial cells
*toxicity∅, Mammary epithelial cells recovered from EGCg treatment even at 50 mM
TumCG↓, growth of HeLa and mammary adenocarcinoma cells was inhibited by EGCg at concentrations as low as 1 mM. With repeated additions of 100 nM EGCg (every 2 hr during the day), growth was inhibited during the day but recovered during the night
NADHdeh?,
eff↑, Green tea infusions were approximately 10 times more effective than those of black tea and contained approximately 10 times more EGCg
ENOX2↓, EGCg inhibit the NADH oxidase(ENOX2) of plasma membrane vesicles from cancer cells and not that of normal cells,
Dose?, with repeated additions (twice daily) at 1 mM EGCg, the EGCg concentration achieving complete inhibition of tNOX in BT-20 cells, growth inhibition and apoptosis in BT-20 cells were achieved.

1516-

EGCG,

Epigallocatechin Gallate (EGCG): Pharmacological Properties, Biological Activities and Therapeutic Potential

Review,

NA,

*Dose∅, A pharmacokinetic study in healthy individuals receiving single doses of EGCGrevealed that plasma concentrations exceeded 1 μM only with doses of >1 g
Half-Life∅, peak levels observed between 1.3 and 2.2 h (and a half-life (t1/2z) of 1.9 to 4.6 h)
BioAv∅, oral bioavailability of 20.3% relative to intravenous admistration
BBB↑, EGCG can cross the blood–brain barrier, allowing it to reach the brain
toxicity∅, Isbrucher et al. found no evidence of genotoxicity in rats following oral administration of EGCG at doses of 500, 1000, or 2000 mg/kg, or intravenous injections of 10, 25, or 50 mg/kg/day.
eff↓, interaction with the folate transporter has been reported, leading to reduced bioavailability of folic acid
Apoptosis↑,
Casp3↑,
Cyt‑c↑, cytochrome c release
cl‑PARP↑,
DNMTs↓,
Telomerase↓,
angioG↓,
Hif1a↓,
NF-kB↓,
MMPs↓,
BAX↑,
Bak↑,
Bcl-2↓,
Bcl-xL↓,
P53↑,
PTEN↑,
IGF-1↓,
H3↓,
HDAC1↓,
*LDH↓, reduces LDL cholesterol, decreases oxidative stress by neutralizing ROS
*ROS↓,

1186-

Gb,

Ginkgolic acid suppresses the development of pancreatic cancer by inhibiting pathways driving lipogenesis

in-vitro,

PC,

in-vitro,

Nor,

HUVECs

in-vivo,

PC,

tumCV↓,
*toxicity∅, little toxicity on normal cells, e.g, HUVEC cells
TumCMig↓,
TumCI↓,
Apoptosis↑,
AMPK↑,
lipoGen↓,
ACC↓,
FASN↓,

2519-

H2,

Hydrogen: an advanced and safest gas option for cancer treatment

Review,

Var,

antiOx↑, H2 has remarkable antioxidant and neuroprotective effects and other advantages
neuroP↓,
BBB↑, swift penetration ability to cross the blood–brain barrier
toxicity∅, H2 inhalation therapy has also been proposed in several countries as the safest mode of H2 administration
TumCP↓, A HeLa xenograft mouse model showed that H2 inhalation may increase the apoptosis rate, proliferation, and oxidative stress in HeLa cells
Apoptosis↓,
ROS↑,
Hif1a↓, H2 may affect tumor growth by regulating the expression of overexpressed subunits of transcription factors, such as hypoxia-inducible factor 1α and the nuclear factor-κB p65 subunit
NF-kB↓,
P53?, Hydrogen also increases the expression level of p53 tumor suppressor proteins.
OS↑, This study revealed that hydrogen gas inhalation 3 h/d can improve the prognosis and overall survival of stage IV colorectal carcinoma patients by decreasing the number of programmed cell death 1/CD8+ T cells
chemoP↑, H 2 anticancer therapy can minimize the debilitating side effects of conventional anticancer therapies by improving survival, quality of life, and blood parameters.

2504-

H2,

Hydrogen gas activates coenzyme Q10 to restore exhausted CD8+ T cells, especially PD-1+Tim3+terminal CD8+ T cells, leading to better nivolumab outcomes in patients with lung cancer

Trial,

Lung,

A total of 42 of 56 patients with lung cancer treated with nivolumab received hydrogen gas

CD8+↑, As previously reported, hydrogen gas improves the prognosis of patients with cancer by restoring exhausted CD8+ T cells into active CD8+ T cells
OS↑, Median survival time (MST) for the HGN-treated patients was 28 months, a length that is approximately 3-fold longer than that for NO-treated patients (MST 9 months)
eff↝, (PDT+ ratio and CoQ10 ratio, respectively) revealed that patients with low PDT+ ratio (<0.81) and high CoQ10 ratio (>1.175) had significantly longer OS compared with those with high PDT+ ratio and low CoQ10 ratio
CoQ10↑, Hydrogen gas has been suggested to enhance the clinical efficacy of nivolumab by increasing CoQ10 (mitochondria) to reduce PDT+, with PDT+ and CoQ10 as reliable negative and positive biomarkers of nivolumab, respectively.
PDT+↓,
PGC-1α↑, As hydrogen gas is reported to activate PGC1-α (14), it is also one of the mitochondrial activation mediators.
Dose↝, Patients were continuously treated with nivolumab (1 mg/kg) every 2 weeks. Patients also inhaled hydrogen gas 3 h daily at their home through a cannula or mask that they rented or purchased and connected to a Hycellvator ET 100
*toxicity∅, Recently, hydrogen gas inhalation was used in patients with post-cardiac arrest syndrome, and adverse events were not observed

3768-

H2,

Effects of Hydrogen Gas Inhalation on Community-Dwelling Adults of Various Ages: A Single-Arm, Open-Label, Prospective Clinical Trial

Trial,

AD,

*ROS↓, Investigation of oxidative stress markers such as reactive oxygen species and nitric oxide showed that their levels decreased post-treatment.
*NO↓,
*BACE↓, BACE-1), amyloid beta (Aβ), r (BDNF), (VEGF-A), T-tau, monocyte chemotactic protein-1 (MCP-1), and inflammatory cytokines (interleukin-6), showed that their cognitive condition significantly improved after treatment, in most cases.
*BDNF↑, see figure 5
*VEGF↑,
*p‑tau↓, t-tau and p-tau levels reduced dramatically in different ages within 4 weeks of treatment;
*MCP1↓, MCP-1 (p < 0.001) (Figure 7A), IL-6 (p < 0.05) (Figure 7B), and VEGF-A (Figure 7C) levels significantly decreased
*IL6↓,
*cognitive↑, H2 gas inhalation may be a good candidate for improving AD with cognitive dysfunction
*toxicity∅, H2 gas inhalation treatment did not cause any adverse effects, indicating that it was safe.

1625-

HCA,

In S. cerevisiae hydroxycitric acid antagonizes chronological aging and apoptosis regardless of citrate lyase

Review,

Nor,

aged yeast cells

CRM↑, Hydroxycitric acid (HCA) is considered a bona fide CRM since it depletes acetyl-CoA pools by acting as a competitive inhibitor of ATP citrate lyase (ACLY), ultimately repressing protein acetylation and promoting autophagy.
ACLY↓, competitive inhibitor of ATP citrate lyase (ACLY)
TumAuto↑, promoting autophagy.
Inflam↓, reduce inflammation and tumour development
TumCG↓,
toxicity∅, HCA appear to have a low or negligible impact in terms of acute or chronic toxicity, genotoxicity, reproductive failure and teratogenicity
lipoGen↓, decreases lipogenesis, insulin resistance, inflammation and oxidative stress
*ROS↓, H2O2 treatment: Strikingly, the molecule was able to largely prevent the massive cell death (PI+ cells) caused by the intense oxidative stress. In parallel there was a sharp increase of live cells with high ROS levels
*OCR↓, chronic exposure to 5 mM HCA (from cell seeding) down-regulated yeast OCR

1631-

HCA,

An overview of the safety and efficacy of a novel, natural(-)-hydroxycitric acid extract (HCA-SX) for weight management

Review,

Obesity,

*ACLY↓, HCA is a competitive inhibitor of ATP citrate lyase
*toxicity∅, No remarkable toxicity results were detected, demonstrating the safety of HCA-SX.
*Dose∅, 4666.7 mg HCA-SX (providing 2,800 mg HCA) in three equally divided doses 30-60 min before meals,

1438-

HCQ,

Chemo,

Adding Chloroquine to Conventional Treatment for Glioblastoma Multiforme

Trial,

GBM,

Chloroquine tablets 150 mg, were commercially purchased
150 mg/d, starting on day 5 after surgery, and was continued for 12 months

30 patients

OS↑, Median survival was 24 months for patients who received chloroquine and 11 months for patients who received placebo.
*toxicity∅, No patient stopped therapy because of toxicity.

2895-

HNK,

Mitochondria-Targeted Honokiol Confers a Striking Inhibitory Effect on Lung Cancer via Inhibiting Complex I Activity

in-vitro,

Lung,

PC9

 0.26 μM

eff↑, Mito-HNK is >100-fold more potent than HNK in inhibiting cell proliferation
TumCP↓,
mt-ROS↑, inhibiting mitochondrial complex ǀ, stimulating reactive oxygen species generation, oxidizing mitochondrial peroxiredoxin-3, and suppressing the phosphorylation of mitoSTAT3
Prx3↑,
mt-STAT3↓,
*toxicity∅, Mito-HNK showed no toxicity and targets the metabolic vulnerabilities of primary and metastatic lung cancers.
selectivity↑,
ChemoSen↑, combination with standard chemotherapeutics.

4639-

HT,

Hydroxytyrosol Induces Apoptosis, Cell Cycle Arrest and Suppresses Multiple Oncogenic Signaling Pathways in Prostate Cancer Cells

in-vitro,

Pca,

LNCaP

in-vitro,

Pca,

C4-2B

TumCP↓, Treatment of LNCaP and C4–2 prostate cancer cells with HT resulted in a dose-dependent inhibition of proliferation
selectivity↑, This was in contrast to HT’s ineffectiveness against normal prostate epithelial cells RWPE1 and PWLE2, suggesting cancer cells-specific effect.
TumCCA↑, HT induced G1/S cell cycle arrest, with inhibition of cyclins D1/E and cdk2/4, and induction of inhibitory p21/p27. HT also induced apoptosis
cycD1/CCND1↓,
cycE/CCNE↓,
CDK2↓,
CDK4↓,
P21↑,
p27↑,
Apoptosis↑, HT also induced apoptosis, as confirmed by flow cytometry, caspase activation, PARP cleavage and BAX/Bcl-2 ratio.
Casp↑,
cl‑PARP↑,
Bax:Bcl2↑, HT inhibits the expression of pro-survival Bcl-2, with concomitant induction of apoptosis-inducing BAX, this tilts the balance in favor of BAX in the cancer cells, marked by increased BAX/Bcl-2 ratio
p‑Akt↓, It inhibited the phosphorylation of Akt / STAT3, and induced cytoplasmic retention of NF-κB,
p‑STAT3↓,
NF-kB↓, transcriptional activity of NF-κB was considerably decreased, dose-dependently, by HT in both the cell lines
AR↓, HT downregulates AR expression
ROS↑, In colon cancer cells, HT has been shown to generate ROS leading to apoptotic cell death and mitochondrial dysfunction. Even in prostate cancer PC3 cells, there is evidence for ROS generation by HT
*BioAv↓, Despite the promising anticancer activity of HT, there have been concerns about its poor bioavailability owing to its extensive metabolism
*toxicity∅, HT is a ‘safe’ compound and can be administered at higher doses without signs of any genotoxic or mutagenic effects

3268-

Lyco,

Lycopene as a Natural Antioxidant Used to Prevent Human Health Disorders

Review,

AD,

*BioAv↓, Lycopene bioavailability can be decreased by ageing, and some of the pathological states, such as cardiovascular diseases (CVDs)
*AntiCan↑, For instance, it has been shown that a higher dietary intake and circulating concentration of lycopene have protective effects against prostate cancer (PCa), in a dose-dependent way
*ROCK1↓, It remarkably lessened the expression of ROCK1, Ki-67, ICAM-1 and ROCK2,
*Ki-67↓,
*ICAM-1↓,
*cardioP↑, Lycopene is a cardioprotective nutraceutical.
*antiOx↑, Lycopene is a well-known antioxidant.
*NQO1↑, Furthermore, lycopene supplementation improves mRNA expressions of the NQO-1 and HO-1 as antioxidant enzymes.
*HO-1↑,
*TNF-α↓, downregulate inflammatory cytokines (i.e., TNF-α, and IL-1β) in the hippocampus of the mice.
*IL22↓,
*NRF2↑, Lycopene decreased neuronal oxidative damage by activating Nrf2, as well as by inactivating NF-κB translocation in H2O2-related SH-SY5Y cell model
*NF-kB↓,
*MDA↓, significantly reduced the malondialdehyde (MDA)
*Catalase↑, Furthermore, it improved the catalase (CAT), superoxide dismutase (SOD), and GSH levels, and antioxidant capacity [109].
*SOD↑,
*GSH↑,
*cognitive↑, Lycopene administration considerably improved cognitive defects, noticeably reduced MDA levels and elevated GSH-Px activity, and remarkably reduced tau
*tau↓,
*hepatoP↑, Lycopene was also found to be effective against hepatotoxicity by acting as an antioxidant, regulating total glutathione (tGSH) and CAT concentrations
*MMP2↑, It also elevated MMP-2 down-regulation
*AST↓, lowering the liver enzymes levels, like aspartate transaminase (AST), alanine transaminase (ALT), LDL, free fatty acid, and MDA.
*ALAT↓,
*P450↑, Moreover, tomato powder has been shown to have a protective agent against alcohol-induced hepatic injury by inducing cytochrome p450 2E1
*DNAdam↓, lycopene decreased DNA damage
*ROS↓, It has been revealed that they inhibited ROS production, protected antioxidant enzymes, and reversed hepatotoxicity in rats’ liver
*neuroP↑, lycopene consumption relieved cognitive defects, age-related memory loss, neuronal damage, and synaptic dysfunction of the brain.
*memory↑,
*Ca+2↓, Lycopene suppressed the 4-AP-invoked release of glutamate and elevated intra-synaptosomal Ca2+ level.
*Dose↝, an in vivo study revealed that lycopene (6.5 mg/day) was effective against cancer in men [147]. However, lycopene dose should be increased up to 10 mg/day, in the case of advanced PCa.
*Dose↑, lycopene supplementation (15 mg/day, for 12 weeks) in an old aged population improved immune function through increasing natural killer cell activity by 28%
*Dose↝, Finally, according to different epidemiological studies, daily lycopene intake can be suggested to be 2 to 20 mg per day
*toxicity∅, A toxicological study on rats showed the no-observed-adverse-effect level at the highest examined dose (i.e., 1.0% in the diet)
PGE2↓, Lycopene doses of 0, 10, 20, and 30 µM were used to treat human colorectal cancer cell. Prostaglandin E2 (PGE2), and NO levels declined after lycopene administration,
CDK2↓, Treatment with lycopene reduced cell hyperproliferation induced by UVB and ultimately promoted apoptosis and reduced CDK2 and CDK4 complex in SKH-1 hairless mice
CDK4↓,
STAT3↓, lycopene reduced the STAT3 expression in ovarian tissues
NOX↓, (SK-Hep-1) cells and indicated a substantial reduction in NOX activity. Moreover, it inhibits the protein expression of NOX4, NOX4 mRNA and ROS intracellular amounts
NOX4↓,
ROS↓,
*SREBP1↓, Lycopene decreases the fatty acid synthase (FAS), sterol regulatory element-binding protein 1c (SREBP-1c), and Acetyl-CoA carboxylase (ACC1) expression in HFD mice.
*FASN↓,
*ACC↓,

1710-

Lyco,

Lycopene: A Natural Arsenal in the War against Oxidative Stress and Cardiovascular Diseases

Review,

CardioV,

antiOx↓, Lycopene is a potent antioxidant that fights ROS and, subsequently, complications.
ROS↓,
BP↓, It reduces blood pressure via inhibiting the angiotensin-converting enzyme and regulating nitrous oxide bioavailability.
LDL↓, important role in lowering of LDL (low-density lipoproteins) and improving HDL (high-density lipoproteins) levels to minimize atherosclerosis
*toxicity∅, Lycopene is a natural substance that may be used in high doses as a dietary supplement without causing harm to human health or physiology
eff↑, Thermal food processing, particularly in the presence of cooking oils, causes lycopene to micellize and enhance its intestinal absorption rate by a factor of ten
ROS↑, As a pro-oxidant, lycopene may have both good and negative impacts in biological systems, as well as influence the course of human illnesses.
*Half-Life↑, Plasma lycopene has a half-life of 12–33 days in the human body
*BioAv↓, Tomato lycopene is not easily absorbed since it is integrated into the nutritional matrix.
*BioAv↑, Clinical research demonstrates that heat-processed tomato products absorb lycopene more quickly than raw sources, and that adding oil increases absorption
*antiOx↑, Lycopene’s ability to protect against oxidative stress has been established

1778-

MEL,

Melatonin: a well-documented antioxidant with conditional pro-oxidant actions

Review,

Var,

Review,

AD,

*ROS↓, melatonin and its metabolic derivatives possess strong free radical scavenging properties.
*antiOx↓, potent antioxidants against both ROS (reactive oxygen species) and RNS (reactive nitrogen species). reduce oxidative damage to lipids, proteins and DNA under a very wide set of conditions where toxic derivatives of oxygen are known to be produced.
ROS↑, a few studies using cultured cells found that melatonin promoted the generation of ROS at pharmacological concentrations (μm to mm range) in several tumor and nontumor cells; thus, melatonin functioned as a conditional pro-oxidant.
selectivity↑, melatonin functions as a prooxidant in cancer cells where it aids in the killing of tumor cells
Dose↑, Melatonin levels in the nucleus and mitochondria reached saturation with a lower dose of 40 mg/kg body weight, with no further accumulation under higher doses of injected melatonin
*mitResp↑, improves mitochondrial respiration and ATP production, thereby reducing electron leakage and ROS generation
*ATP↑,
*ROS↓,
eff↑, melatonin protects mitochondrial function in the brain of Alzheimer's patients through both MT1/MT2 dependent and independent mechanisms
ROS↑, Cytochrome P450 utilizes melatonin as a substrate to generate ROS in mitochondria (melatonin concentration ranges from 0.1 to 10 uM)
Dose↑, melatonin at high concentrations (10-1000uM ) was able to promote ROS generation and lead to Fas-induced apoptosis in human leukemic Jurkat cells. Concentrations of <10uM , melatonin did not induce significant ROS generation in these cancer cells
*toxicity∅, High levels of melatonin (uM to mM) did not cause cytotoxicity in several types of nontumor cells
ROS↑, lower concentrations of melatonin (0.1-10uM ), which exhibited antioxidant action in HepG2 cells within 24 hr, became pro-oxidant after 96 hr of treatment, as indicated by the increase of GSH with 24hr and depletion after 96 hr.
eff↓, Finally, a compound, chlorpromazine, which specifically interrupts the binding of melatonin to calmodulin [188], prevented melatonin-induced AA release and ROS generation;
ROS↝, It remains unknown whether the pro-oxidant action exists in vivo. the vast majority of evidence indicates that melatonin is a potent antioxidant in vivo even at pharmacological concentrations
Dose↑, decline of melatonin production with age may render it more beneficial to supplement melatonin to the aging population to improve health by reducing free radical damage
other↑, melatonin intake has the potential to improve cardiac function, inhibit cataract formation, maintain brain health, alleviate metabolic syndrome, obesity and diabetes,reduce tumorigenesis, protect tissues against ischemia

1777-

MEL,

Melatonin as an antioxidant: under promises but over delivers

Review,

NA,

*ROS↓, uncommonly effective in reducing oxidative stress under a remarkably large number of circumstances
*Fenton↓, reportedly chelates transition metals, which are involved in the Fenton/Haber-Weiss reactions
*antiOx↑, credible evidence to suggest that melatonin should be classified as a mitochondria-targeted antioxidant
*toxicity∅, uncommonly high-safety profile of melatonin also bolsters this conclusion.
*GPx↑, melatonin was found to stimulate antioxidative enzymes including glutathione peroxidase and glutathione reductase
*GSR↑,
*GSH↑, melatonin upregulates the synthesis of glutathione
*NO↓, neutralize nitrogen-based toxicants, i.e., nitric oxide
*Iron↓, Melatonin chelates both iron (III) and iron (II), which is the form that participates in the Fenton reaction to generate the hydroxyl radical
*Copper↓, copper-chelating ability of melaton
*IL1β↓, significant reductions in plasma cardiac troponin 1, interleukin 1 beta, inducible nitric oxide synthase (iNOS) and caspase 3 due to melatonin
*iNOS↓,
*Casp3↓,
*BBB↑, melatonin readily crosses the blood-brain barrier;
*RenoP↑, Published reports haveshown that the lung,231, 232 liver, 233- 235 kidney,236 pancreas,237 intestine,238 urinary bladder,239,240 corpus cavernosum,241 skeletal muscle242, 243 spinal cord244, 245 and stem cells246 are alsoprotected by melatonin.
chemoP↑, Melatonin has not been found to interfere with the efficacy of prescription drugs. Doxorubicin, if given it in combination with melatonin may allow the use of a larger dose with greater efficacy.
*Ca+2↝, Moreover, melatonin regulates free Ca2+ movement intracellularly
eff↑, elatonin was found to exaggerate the cancer inhibiting actions of pitavastatin270 and pravastatin271 against breast cancer in experimental studies
*PKCδ?, major targets by which melatonin reduces methamphetamine-related neuronal damage is due to the inhibition of the PKCδ gene
ChemoSen↑, at least some cases melatonin reduces the toxicity of these pharmacological agents in normal cells256, 289, 290 while enhancing the cancer-killing actions (also, see below) of conventional chemotherapeutic agents.256, 291-293
eff↑, TRAIL was combined with melatonin for the treatment of A172 and U87 human glioblastoma cells, however, apoptotic cell death was greatly exaggerated over that caused by TRAIL alone
Akt↓, in GBM: observed effect was related to a modulation of protein kinase c which reduced Akt activation resulting in a rise in death receptor 5 (DR5) levels;
DR5↑,
selectivity↑, The pro-oxidant action of melatonin is common in cancer cells while in normal cells the indoleamine is a powerful antioxidant.
ROS↑, cancer cells
eff↑, human lung adenocarcinoma cells (SK-LV-1) showed that melatonin also increased their sensitivity to the chemotherapy, cisplatin.

2260-

MF,

Alternative magnetic field exposure suppresses tumor growth via metabolic reprogramming

in-vitro,

GBM,

U87MG

18 mT at the center

in-vitro,

GBM,

LN229

in-vivo,

NA,

AMF for 30 min daily, for a total of five sessions.

mice

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.

3536-

MF,

Targeting Mesenchymal Stromal Cells/Pericytes (MSCs) With Pulsed Electromagnetic Field (PEMF) Has the Potential to Treat Rheumatoid Arthritis

Review,

Arthritis,

Review,

Stroke,

*Inflam↓, (PEMF), a biophysical form of stimulation, has an anti-inflammatory effect by causing differentiation of MSCs.
*Diff↑,
*toxicity∅, PEMF have been reported to last up to 3 months or longer in human patients with chronic inflammatory/autoimmune disorders (38) with no evidence of adverse effects (39).
*other↑, MSCs to promote immunomodulation and improve cartilage and bone regeneration in vitro (10) and in vivo (73).
*SOX9↑, enhanced chondrogenic gene expression in SOX-9, COL II, and aggrecan in MSCs
*COL2A1↑,
*NO↓, Prevented increases in NO
*PGE2↓, Exposure to PEMF induces early upregulation of adenosine receptors A2A and A3 that reduce PGE2 and pro-inflammatory cytokines such as TNF-α, which combine to inhibit the activation of transcription factor NF-kB
*NF-kB↓,
*TNF-α↓, 1 h exposure to PEMF has been shown to down-regulate both NF-kB and TNF-α in murine macrophages
*IL1β↓, By inhibiting NF-kB activation (94), exposure to PEMF led to decreased production of TNF-α, IL-1β, IL-6, and PGE2 in human chondrocytes, osteoblasts, and synovial fibroblasts
*IL6↓,
*IL10↑, Inhibited release of PGE2, and IL-1β and IL-6 production, while stimulating release of IL-10 in synovial fibroblasts
*angioG↑, progenitor cells (EPCs) to an RA injury site is important for repair of vasculature and angiogenesis. PEMF has also been reported to increase the number and function of circulating EPCs in treating myocardial ischemia/reperfusion (I/R) injury in rat
*MSCs↑, Since PEMF have been shown to stimulate the production of MSCs
*VEGF↑, promoting the expression of growth factors such as VEGF and TGF-β
*TGF-β↑,
*angioG↝, modulate the aberrant angiogenesis present in RA: reported to significantly reduce activation levels of VEGF (15), to inhibit the proliferative ability of HUVECs, and to reduce the extent of vascularization in diseased tissue
*VEGF↓, diseased tissue
Ca+2↝, By restoring normal Ca2+ ion flux and Na+/K+ balance, the cell can begin the process of down-regulating inflammatory cytokines, HSPs, and proangiogenic molecules such as VEGF, making it possible for the body to commence rebuilding healthy cartilage.

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,

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.

3475-

MF,

A Pulsed Electromagnetic Field Protects against Glutamate-Induced Excitotoxicity by Modulating the Endocannabinoid System in HT22 Cells

in-vitro,

Nor,

HT22

Review,

AD,

*Apoptosis↓, PEMF exposure improved viability of HT22 cells after excitotoxicity and reduced lactate dehydrogenase release and cell death.
*LDH↓,
*neuroP↑, PEMF exposure indicated that the neuroprotective effects of PEMF were related to modulation of the eCB metabolic system.
*toxicity∅, Recent studies have shown that PEMF is a safe and non-invasive approach for management of several neurological diseases, including Alzheimer's disease
*IL1β↓, Previous studies have shown that PEMF could modulate inflammation after traumatic brain injury by inhibiting production of pro-inflammatory factor IL-1β
*Inflam↓, PEMF influences neuroinflammation via elevation of anti-inflammatory IL-10 and reduction of pro-apoptotic tumor necrosis factor
*IL10↑,
*TNF-α↓,

Showing Research Papers: 1 to 50 of 84
Page 1 of 2 Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 84

Pathway results for Effect on Cancer / Diseased Cells:

Infection & Microbiome ⓘ

CD8+↑, 1,
Total Targets: 204

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↓, 1, antiOx↑, 9, Catalase↑, 2, Copper↓, 1, Fenton↓, 1, GPx↑, 2, GSH↑, 4, GSR↑, 1, H2O2∅, 1, HO-1↑, 2, Iron↓, 1, lipid-P↓, 3, MDA↓, 2, NQO1↑, 1, NQO1∅, 1, NRF2↓, 1, NRF2↑, 2, OXPHOS↑, 1, ROS↓, 12, ROS∅, 2, SOD↑, 3,

Metal & Cofactor Biology ⓘ

IronCh↑, 2,

Mitochondria & Bioenergetics ⓘ

ATP↑, 1, mitResp↑, 1, OCR↓, 1,

Core Metabolism/Glycolysis ⓘ

ACC↓, 1, Acetyl-CoA↑, 1, ACLY↓, 1, ALAT↓, 1, FASN↓, 1, LDH↓, 2, SREBP1↓, 1,

Cell Death ⓘ

Apoptosis↓, 1, Casp3↓, 1, iNOS↓, 1,

Kinase & Signal Transduction ⓘ

SOX9↑, 1,

Transcription & Epigenetics ⓘ

other↑, 1,

DNA Damage & Repair ⓘ

DNAdam↓, 1,

Cell Cycle & Senescence ⓘ

TumCCA↑, 1,

Proliferation, Differentiation & Cell State ⓘ

Diff↑, 1, MSCs↑, 1,

Migration ⓘ

AP-1↓, 1, Ca+2↓, 1, Ca+2↝, 1, COL2A1↑, 1, Ki-67↓, 1, MMP2↑, 1, PKCδ?, 1, ROCK1↓, 1, TGF-β↑, 1,

Angiogenesis & Vasculature ⓘ

angioG↑, 1, angioG↝, 1, NO↓, 3, VEGF↓, 1, VEGF↑, 2,

Barriers & Transport ⓘ

BBB↑, 3, BBB↝, 1,

Immune & Inflammatory Signaling ⓘ

COX2↓, 1, ICAM-1↓, 1, IL10↑, 2, IL1α∅, 1, IL1β↓, 4, IL1β∅, 1, IL22↓, 1, IL6↓, 2, IL8∅, 1, Inflam↓, 4, MCP1↓, 1, MCP1∅, 1, NF-kB↓, 3, PGE2↓, 1, TNF-α↓, 4,

Synaptic & Neurotransmission ⓘ

AChE↓, 1, BDNF↑, 1, ChAT↑, 1, tau↓, 1, p‑tau↓, 1,

Protein Aggregation ⓘ

Aβ↓, 2, BACE↓, 1,

Drug Metabolism & Resistance ⓘ

BioAv↓, 7, BioAv↑, 4, BioAv↝, 2, Dose↑, 1, Dose↝, 7, Dose∅, 2, eff↑, 1, Half-Life↑, 1, Half-Life↝, 1, P450↑, 1,

Clinical Biomarkers ⓘ

ALAT↓, 1, AST↓, 1, IL6↓, 2, Ki-67↓, 1, LDH↓, 2,

Functional Outcomes ⓘ

AntiCan↑, 1, AntiDiabetic↑, 1, cardioP↑, 2, cognitive↑, 4, cognitive∅, 1, hepatoP↑, 2, memory↑, 4, neuroP↑, 5, RenoP↑, 1, toxicity∅, 42,
Total Targets: 104

Scientific Paper Hit Count for: toxicity, toxicity

8 Magnetic Fields
4 Chemotherapy
4 Dichloroacetate
4 Magnetic Field Rotating
4 Sulforaphane (mainly Broccoli)
3 Apigenin (mainly Parsley)
3 Ellagic acid
3 EGCG (Epigallocatechin Gallate)
3 Hydrogen Gas
3 Propolis -bee glue
3 Vitamin K2
2 Allicin (mainly Garlic)
2 Baicalein
2 Carnosine
2 Metformin
2 diet FMD Fasting Mimicking Diet
2 Oxygen, Hyperbaric
2 HydroxyCitric Acid
2 Lycopene
2 Melatonin
2 Pterostilbene
2 Silymarin (Milk Thistle) silibinin
2 Shikonin
2 Whole Body Vibration
1 Silver-NanoParticles
1 Alpha-Lipoic-Acid
1 Anti-oxidants
1 Astaxanthin
1 Bacopa monnieri
1 Capsaicin
1 Carvacrol
1 Citric Acid
1 Copper and Cu NanoParticles
1 Black phosphorus
1 SonoDynamic Therapy UltraSound
1 Curcumin
1 Deguelin
1 diet Ketogenic
1 Ginkgo biloba
1 hydroxychloroquine
1 Honokiol
1 HydroxyTyrosol
1 immunotherapy
1 Mushroom Lion’s Mane
1 Naringin
1 Oleuropein
1 5-fluorouracil
1 sericin
1 Propyl gallate
1 Piperlongumine
1 Sanguinarine
1 Resveratrol
1 EMF
1 Rosmarinic acid
1 Selenite (Sodium)
1 Radiotherapy/Radiation
1 Thymoquinone
1 Thymol-Thymus vulgaris

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#:%  Target#:1025  State#:%  Dir#:6
  wNotes=on  sortOrder:rid,rpid

toxicity Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Metal & Cofactor Biology ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Cellular Microenvironment ⓘ

Hormonal & Nuclear Receptors ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Metal & Cofactor Biology ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Kinase & Signal Transduction ⓘ

Transcription & Epigenetics ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Synaptic & Neurotransmission ⓘ

Protein Aggregation ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

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