NADH Cancer Research Results

NADH, Nicotinamide Adenine Dinucleotide: Click to Expand ⟱
Source:
Type:
NADH is the reduced form of NAD⁺, meaning it has accepted electrons (and usually a proton) during metabolic reactions. When NAD⁺ accepts electrons (typically during metabolic processes like glycolysis, the citric acid cycle, and beta-oxidation), it becomes NADH.
-By influencing the balance between NADH and NAD⁺, ENOX2 might shift the cellular redox state. An imbalance can lead to increased oxidative stress or changes in ROS signaling pathways.

• The ratio between NADH and NAD⁺ is a key indicator of a cell’s metabolic state.
• Some studies have suggested that abnormal NADH metabolism or shifts in the NADH/NAD⁺ ratio can be correlated with tumor aggressiveness or response to therapy.
• For example, in certain cancers, a higher NADH/NAD⁺ ratio may be associated with more aggressive behavior, resistance to apoptosis, or poor prognosis.
Scientific Papers found: Click to Expand⟱
175- Api,    Apigenin up-regulates transgelin and inhibits invasion and migration of colorectal cancer through decreased phosphorylation of AKT
- vitro+vivo, CRC, SW480 - vitro+vivo, CRC, DLD1 - vitro+vivo, CRC, LS174T
MMP↓,
p‑Akt↓,
TumCP↓, Apigenin inhibits cell proliferation and invasion
TumCI↓,
NADH↓, down-regulated proteins by apigenin included NADH dehydrogenase [ubiquinone] iron-sulphur protein 3, heat shock protein HSP 90-alpha, stress-70 protein and NADH dehydrogenase
HSP90↓,
other↑, whereas the up-regulated proteins include Transgelin, Ras-related protein Rab-3D and 28S ribosomal protein S22
talin?,

5833- CAP,    Capsaicin: From Plants to a Cancer-Suppressing Agent
- Review, Var, NA
chemoPv↑, it has been found that capsaicin can act as a cancer preventive agent and shows wide applications against various types of cancer.
TumCCA↑, The proposed anticancer mechanisms of capsaicin include an increase of cell-cycle arrest and apoptosis
Apoptosis↑,
ROS↑, Colo 205 150 Induced cell death, increased ROS and pro-apoptotic proteins
MMP↓, Human bladder cancer T24 100 Induced ROS production and mitochondrial membrane depolarization
Ca+2↑, capsaicin induces apoptosis in cancer cells is not completely elucidated but involves intracellular calcium increase, ROS, disruption of mitochondrial membrane transition potential, and activation of transcription factors such as NFκB and STATS (
JNK↑, studies performed in pancreatic cells showed that capsaicin apoptosis inducing effects were associated with ROS generation, JNK activation, mitochondrial depolarization, release of cytochrome c in the cytosol and activation of caspase-3 cascade
Casp3↑,
NADH↓, Capsaicin can also inhibit the plasma membrane NADH oxidase by functioning as a coenzyme Q antagonist.
CDK2↓, Capsaicin inhibits the proliferation of 5637 bladder carcinoma cells by cycle arrest with the inhibition of CDK2, CDK4 and CDK6.
CDK4↓,
CDK6↓,
P53↑, capsaicin induces apoptosis in AGS cells through upregulation of p53 and that the apoptotic activity of capsaicin is p53-dependent.

5858- CAP,    Capsaicin as a Microbiome Modulator: Metabolic Interactions and Implications for Host Health
- Review, Nor, NA - Review, AD, NA
*BBB↓, crosses the blood–brain barrier, alters neurotransmitter levels, and accumulates in brain regions involved in cognition.
*GutMicro↑, capsaicin appears to undergo microbial transformation and influences gut microbial composition, favoring short-chain fatty acid producers and suppressing pro-inflammatory taxa. often favoring the growth of beneficial taxa such as Ruminococcaceae, Lac
Obesity↓, These changes contribute to anti-obesity, anti-inflammatory, and potentially anticancer effects
*Inflam↓,
*AntiCan↑,
*TRPV1↑, Capsaicin is a potent agonist perceived by TRPV1, a transmembrane cation channel that functions with Ca2+.
*Ca+2↑, causes an increase in Ca2+ flux,
*antiOx↑, Capsaicin is a bioactive compound of chili peppers responsible for their spicy flavor, which also shows antioxidant, anti-obesity, analgesic, anti-inflammatory, anticarcinogenic, and cardioprotective effects
*cardioP↑,
*BioAv↓, capsaicin exhibits low systemic bioavailability due to its rapid metabolism in the liver and other tissues, resulting in a short plasma half-life of approximately 25 min in humans
*Half-Life↓,
*BioAv↝, Capsaicin’s bioavailability is determined by multiple interrelated factors, including its physicochemical properties, metabolic transformations, route of administration, and the biological context of the host, including gut microbiota composition.
*BioAv↑, For instance, polymeric micelles, liposomes, and hydroxypropyl-β-cyclodextrin complexes have demonstrated the capacity to enhance capsaicin’s oral bioavailability, prolong its plasma half-life, and improve therapeutic consistency
*neuroP↑, capsaicin exposure alters glutamate, GABA, and serotonin levels in distinct brain regions, with potential implications for neuroprotection, mood regulation, and energy metabolism.
Apoptosis↑, apoptosis is the main mechanism by which capsaicin induces cell death in cancer cells.
p38↑, capsaicin triggers a calcium flux within the cell via TRPV1, activating the p38 pathway.
ROS↑, As a result, reactive oxygen species (ROS) are produced, along with depolarization of the mitochondrial membrane potential and opening of the mitochondrial permeability transition pore.
MMP↓,
MPT↑,
Cyt‑c↑, Consequently, cytochrome c is released, the apoptosome is assembled, and caspases are activated, ultimately leading to cell death
Casp↑,
TRIB3↑, capsaicin enhances TRIB3 gene expression, which allowed an increase in the antiproliferative and proapoptotic effects of TRIB3 in cancer cells
NADH↓, Capsaicin has also been seen to downregulate and inhibit tumor-associated NADH oxidase (tNOX) and Sirtuin1 (SIRT1) in multiple cancer cell lines such as bladder cancer, which led to reduced cell growth and migration
SIRT1↓,
TumCG↓,
TumCMig↓,
TOP1↓, pointing out that capsaicin had an inhibitory effect on topoisomerases I and II, causing a reduction in metabolic activity and proliferation of a human colon cancer cell line
TOP2↓,
β-catenin/ZEB1↓, with capsaicin, the β-catenin transcription gets downregulated
*ROS↓, Capsaicin has also been proven to alleviate redox imbalance or oxidative stress, thanks to its antioxidative activity.
*Aβ↓, Alsheimer’s disease, attenuating neurodegeneration in mice by reducing amyloid-beta levels via the promotion of non-amyloidogenic processing of amyloid precursor protein

1586- Citrate,    Extracellular Citrate Is a Trojan Horse for Cancer Cells
- in-vitro, Liver, HepG2
Dose?, At low concentration, citrate increased both histone H4 acetylation and lipid deposition; at high concentration, citrate inhibited both
ac‑H4↓,
lipidDe↓,
ACLY↓, Considering the strong demand for acetyl-CoA but not for OAA in tumor cells, the exogenous citrate would behave like a trojan horse that carries OAA inside the cells and reduces ACLY expression and cellular metabolism.
selectivity↑, in non-tumor cells, changes of acetylated histone level do not correspond to a change of ACLY expression, as instead shown by HepG2 cells.
*ACLY∅, In contrast, ACLY expression in IHH (normal)cells was not modified after citrate exposure, suggesting that, in this case, ACLY expression was not regulated by histone H4 acetylation
Glycolysis↓, strong inhibition of glycolysis, which leads to a decrease in NADH necessary for OAA reduction
NADH↓,
OAA↑, exogenous citrate would behave like a trojan horse that releases OAA in the cells, where it could exert its therapeutic effect also on hepatoma cells.
other↑, most important discovery is undoubtedly the demonstration that high concentrations of citrate decrease the availability of acetyl-CoA, a key molecule both in the metabolism of sugars and lipids

1891- MGO,    Methylglyoxal induces mitochondria-dependent apoptosis in sarcoma
- in-vitro, SCC, NA
NADH↓, It appears that this specificity of methylglyoxal against the NADH dehydrogenase (complex I) of malignant tissue mitochondria is one very important reason for its selective anticancer property.
MMP↓, decrease in membrane potential
Cyt‑c↑, Release of cytochrome c from sarcoma tissue mitochondria.
selectivity↑, The results presented in this and the preceding paper clearly indicate that action of methylglyoxal is selective against malignant cells
Apoptosis↑, Methylglyoxal showed cytotoxicity to several malignant cells through induction of apoptosis
ROS↑, It was previously reported that methylglyoxal induced ROS generation triggered apoptosis in human Hep G2 cells
ATP↓, ATP deprivation

5904- TV,    Pharmacological Properties and Molecular Mechanisms of Thymol: Prospects for Its Therapeutic Potential and Pharmaceutical Development
- Review, Var, NA - Review, Stroke, NA - Review, Diabetic, NA - Review, Obesity, NA - Review, AD, NA - Review, Arthritis, NA
*antiOx↑, shown to possess various pharmacological properties including antioxidant, free radical scavenging, anti-inflammatory, analgesic, antispasmodic, antibacterial, antifungal, antiseptic and antitumor activities.
*ROS↓,
*Inflam↓,
*Bacteria↓,
AntiTum↑,
IronCh↑, chelation of metal ions
*HDL↑, antihyperlipidemic (via increasing the levels of high density lipoprotein cholesterol and decreasing the levels of low density lipoprotein cholesterol
*LDL↓,
*BioAv↝, videnced the presence of thymol in the stomach, intestine, and urine after its oral administration with sesame oil at a dose around 500 mg in rats and 1–3 g in rabbits.
*Half-Life↝, Oral administration of a single dose of thymol (50 mg/kg) was rapidly absorbed and slowly eliminated approximately within 24 h.The maximum concentration (Tmax) was reached after 30 min, while approximately 0.3 h was needed for the half-life
*BioAv↑, The rapid absorption of thymol indicates that it’s mainly absorbed in the upper component of the gut
*SOD↑, scavenging of free radicals by increasing the activities of several endogenous antioxidant enzymes levels viz. superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), glutathione-S-transferase (GST)
*GPx↑,
*GSTs↑,
*eff↑, Thymol (0.02–0.20%) showed better antioxidant capacity than its isomer carvacrol in lipid systems due to its greater steric hindrance
radioP↑, Owing to its potent antioxidant potential, thymol showed radioprotective and anticlastogenic potential in gamma radiation induced Swiss albino mice
*MDA↓, Thymol supplementation increased the antioxidant status and decreased malondialdehyde (MDA) levels in broiler chickens
*other↑, Dietary supplementation with the combination of carvacrol–thymol (1:1) (100 mg/kg) reduced the occurrence of oxidative stress and the impairment of the intestinal barrier in weaning piglets by its potent antioxidant property
*COX1↓, by inhibiting both isoforms of cyclooxygenase (COX), with the most active being against COX-1 with an IC50 value of 0.2 μM.
*COX2↓,
*AntiAg↑, Thymol (1.1 μg/ml) exhibited inhibitory effects against arachidonic-acid-induced blood coagulation and platelet aggregation in vitro
*RNS↓, Thymol inhibited ROS (IC50= 3 μg/ml), reactive nitrogen species (RNS) (IC50= 4.7) and significantly reduced generation of NO and H2O2 as well as activities of nitric oxide synthase (NOS) and nicotinamide adenine dinucleotide reduced oxidase (NADH oxi
*NO↓,
*H2O2↓,
*NOS2↓,
*NADH↓,
*Imm↑, Thymol (25–200 mg/kg) was shown to modulate the immune system in cyclosporine-A treated Swiss albino mice by enhancing the expressions of cluster of differentiation 4 (CD4),
Apoptosis↑, anticancer actions of thymol include induction of apoptosis, anti-proliferation, inhibition of angiogenesis and migration
TumCP↓,
angioG↓,
TumCMig↓,
Ca+2↑, Intracellular Ca2+ overload
TumCCA↑, Cytotoxicity by stimulating cell cycle arrest in G0/G1 phase
DNAdam↑, DNA fragmentation, Bax protein expression, activation of caspase -9, -8 and -3 & concomitant PARP cleavage, AIF translocation
BAX↑,
Casp9↑,
Casp8↑,
Casp3↑,
cl‑PARP↑,
AIF↑,
i-ROS↑, intracellular ROS, depolarizing MMP, cytochrome-c release, cleavage of caspases, DNA fragmentation, activation of apaf-1,
MMP↓,
Cyt‑c↑,
APAF1↑,
Ca+2↑, In human glioblastoma cells, thymol (200–600 μM) produced a rise in (Ca2+)i levels
MMP9↓, diminished matrix metallopeptidase-9 (MMP9) and matrix metallopeptidase-2 (MMP2) production as well as protein kinase Cα (PKCα) and extracellular signal-regulated kinases (ERK1/2) phosphorylation
MMP2↓,
PKCδ↓,
ERK↓,
H2O2↑, Thymol increased the production of ROS and mitochondrial H2O2 thereby depolarizing mitochondrial membrane potential.
BAX↑, up-regulating Bcl-2 associated X protein (Bax) expression and down-regulating B-cell lymphoma (Bcl-2)
Bcl-2↓,
DNAdam↑, Thymol (IC50= 497 and 266 mM) was shown to induce DNA damage by increasing the levels of lipid peroxidation products;
lipid-P↑,
ChemoSen↑, This study recommended the combination of thymol with various chemotherapeutic agents to minimize its toxicity on normal cells and to improve the effectiveness of cancer treatment
chemoP↑,
*cardioP↑, significant increase in the activities of heart mitochondrial antioxidants (SOD, catalase, GPx, GSH)
*SOD↑,
*Catalase↑,
*GPx↑,
*GSH↑,
*BP↓, Thymol (1, 3, and 10 mg/kg) administration decreased the blood pressure and heart rate of Wistar rats whereas thymol (5 mg/kg) attenuated blood pressure in rabbits
*AntiDiabetic↑, protective effects of thymol in metabolic disorders such as diabetes mellitus and obesity
*Obesity↓,
RenoP↑, Thymol (20 mg/kg) was shown to inhibit cisplatin-induced renal injury by attenuating oxidative stress, inflammation and apoptosis in male adult Swiss Albino rats
*GastroP↑, This gastroprotective effect of thymol is believed to be due to increased mucus secretion
hepatoP↑, Thymol (150 mg/kg) showed to inhibit paracetamol induced hepatotoxicity in mice by preventing the alterations in the activities of hepatic marker enzymes
*AChE↓, Thymol (EC50= 0.74 mg/mL) was shown to possess acetylcholine esterase inhibitory activity but much less than its isomer carvacrol
*cognitive↑, Thymol (0.5–2 mg/kg) has been shown to inhibit cognitive impairments caused by increased Aβ levels or cholinergic hypofunction in Aβ
*BChE↓, whereas thymol (100 and 1000 μg/ml) also inhibited both AChE and butyrylcholinesterase (BChE) in a dose dependent manner
*other↓, Thymol (100 mg/kg) was shown to inhibit collagen induced arthritis by decreasing lipid peroxidation mediated oxidative stress by increasing the status of antioxidants in male Wistar rats
*BioAv↑, The encapsulation of thymol into methylcellulose microspheres by spray drying remarkably increases the bioavailability compared to free thymol


Showing Research Papers: 1 to 6 of 6

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 6

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

H2O2↑, 1,   lipid-P↑, 1,   lipidDe↓, 1,   NADH↓, 5,   ROS↑, 3,   i-ROS↑, 1,  

Metal & Cofactor Biology ⓘ

IronCh↑, 1,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 1,   ATP↓, 1,   MMP↓, 5,   MPT↑, 1,  

Core Metabolism/Glycolysis ⓘ

ACLY↓, 1,   Glycolysis↓, 1,   OAA↑, 1,   SIRT1↓, 1,  

Cell Death ⓘ

p‑Akt↓, 1,   APAF1↑, 1,   Apoptosis↑, 4,   BAX↑, 2,   Bcl-2↓, 1,   Casp↑, 1,   Casp3↑, 2,   Casp8↑, 1,   Casp9↑, 1,   Cyt‑c↑, 3,   JNK↑, 1,   p38↑, 1,  

Transcription & Epigenetics ⓘ

ac‑H4↓, 1,   other↑, 2,  

Protein Folding & ER Stress ⓘ

HSP90↓, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 2,   P53↑, 1,   cl‑PARP↑, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   CDK4↓, 1,   TumCCA↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

ERK↓, 1,   TOP1↓, 1,   TOP2↓, 1,   TumCG↓, 1,  

Migration ⓘ

Ca+2↑, 3,   MMP2↓, 1,   MMP9↓, 1,   PKCδ↓, 1,   talin?, 1,   TRIB3↑, 1,   TumCI↓, 1,   TumCMig↓, 2,   TumCP↓, 2,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,  

Hormonal & Nuclear Receptors ⓘ

CDK6↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,   Dose?, 1,   selectivity↑, 2,  

Clinical Biomarkers ⓘ

TRIB3↑, 1,  

Functional Outcomes ⓘ

AntiTum↑, 1,   chemoP↑, 1,   chemoPv↑, 1,   hepatoP↑, 1,   Obesity↓, 1,   radioP↑, 1,   RenoP↑, 1,  
Total Targets: 63

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 2,   Catalase↑, 1,   GPx↑, 2,   GSH↑, 1,   GSTs↑, 1,   H2O2↓, 1,   HDL↑, 1,   MDA↓, 1,   NADH↓, 1,   RNS↓, 1,   ROS↓, 2,   SOD↑, 2,  

Core Metabolism/Glycolysis ⓘ

ACLY∅, 1,   LDL↓, 1,  

Cell Death ⓘ

TRPV1↑, 1,  

Transcription & Epigenetics ⓘ

other↓, 1,   other↑, 1,  

Migration ⓘ

AntiAg↑, 1,   Ca+2↑, 1,  

Angiogenesis & Vasculature ⓘ

NO↓, 1,  

Barriers & Transport ⓘ

BBB↓, 1,   GastroP↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX1↓, 1,   COX2↓, 1,   Imm↑, 1,   Inflam↓, 2,  

Synaptic & Neurotransmission ⓘ

AChE↓, 1,   BChE↓, 1,  

Protein Aggregation ⓘ

Aβ↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 3,   BioAv↝, 2,   eff↑, 1,   Half-Life↓, 1,   Half-Life↝, 1,  

Clinical Biomarkers ⓘ

BP↓, 1,   GutMicro↑, 1,   NOS2↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   AntiDiabetic↑, 1,   cardioP↑, 2,   cognitive↑, 1,   neuroP↑, 1,   Obesity↓, 1,  

Infection & Microbiome ⓘ

Bacteria↓, 1,  
Total Targets: 45

Scientific Paper Hit Count for: NADH, Nicotinamide Adenine Dinucleotide
2 Capsaicin
1 Apigenin (mainly Parsley)
1 Citric Acid
1 Methylglyoxal
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#:1120  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

 

Home Page