NH3 Cancer Research Results

NH3, ammonia: Click to Expand ⟱
Source:
Type:
Cancer cells can produce ammonia through processes like glutaminolysis, where glutamine is metabolized to support rapid growth and proliferation.
High levels of ammonia can suppress the function of certain immune cells, such as T cells and natural killer (NK) cells, potentially allowing tumors to evade immune surveillance.
Scientific Papers found: Click to Expand⟱
8108- L-Orn,    Safety assessment of L-ornithine oral intake in healthy subjects: a systematic review
- Review, Nor, NA
*toxicity↓, 14,025 mg/person/day in the form of L-Orn hydrochloride and the maximum duration of administration was 156 days.
*toxicity↓, the no observed adverse effect level was estimated to be 12,000 mg/person/day for L-Orn in the form of L-Orn hydrochloride.
*GH↑, , its ingestion leads to the release of growth hormone
*Obesity↓, In addition, the ingestion of L-Orn and L-arginine with exercise loading was reported to decrease weight and body fat (Elam 1988) and increase lean body mass in healthy men
*NH3↓, it is used for pharmacological treatment to decrease blood ammonia concentrations and to reduce the symptoms of hepatic encephalopathy associated with liver cirrhosis
*hepatoP↑, L-Orn has also been reported to promote alcohol metabolism in the liver, suppress ethanol-induced hepatocellular death, and improve sleep quality after drinking
*Sleep↑,
*fatigue↓, In human studies, L-Orn administration has been reported to improve physical fatigue (Demura et al. 2011) and to suppress the elevation of blood ammonia during exercise

8110- L-Orn,    L-ornithine supplementation attenuates physical fatigue in healthy volunteers by modulating lipid and amino acid metabolism
- Trial, Nor, NA
*Dose↝, 17 healthy volunteers were randomized to L-ornithine (2000 mg/d for 7 days and 6000 mg/d for 1 day as L-ornithine hydrochloride) or placebo for 8 days
*KeyT↝, oral L-ornithine administration promoted lipid metabolism and activated the urea cycle from serum triacylglycerol, ketone bodies, free fatty acids, and blood ammonia level changing.
*FFA/NEFA↝,
*NH3↓,
*fatigue↓, L-ornithine significantly attenuated the subjective feeling of fatigue

2068- PB,    Phenylbutyrate-induced glutamine depletion in humans: effect on leucine metabolism
- in-vivo, Nor, NA
glut↓, The 24-h phenylbutyrate treatment was associated with 1) an ≈26% decline in plasma glutamine concentration from 514 ± 24 to 380 ± 15 μM (means ± SE; P < 0.01 with pairedt-test) with no change in glutamine appearance rate or de novo synthesis;2)
NH3↓, Phenylacetate in turn reacts with glutamine in liver and kidney to yield phenylacetylglutamine (Fig.1). The latter is quantitatively excreted as such in the urine and seems to substitute for urea as a means to eliminate excess ammonia
eff↝, it is not known whether large doses of phenylbutyrate alter plasma glutamine concentration in healthy adults with an intact urea synthetic pathway

2048- PB,    Sodium Phenylbutyrate Inhibits Tumor Growth and the Epithelial-Mesenchymal Transition of Oral Squamous Cell Carcinoma In Vitro and In Vivo
- in-vitro, OS, CAL27 - in-vitro, Oral, HSC3 - in-vitro, OS, SCC4 - in-vivo, NA, NA
*NH3↓, Sodium phenylbutyrate (SPB) as a salt of 4-phenylbutyric acid (4-PBA) has been reported to be an ammonia scavenger, histone deacetylase inhibitor, and an endoplasmic reticulum stress inhibitor
*HDAC↓,
*ER Stress↓,
Apoptosis?, SPB could significantly promote cell apoptosis
Bcl-2↓, BCL-2 was downregulated
cl‑Casp3↑, cleavage of caspase-3 was increased
TGF-β↑, transforming growth factor-β (TGFB) related epithelial-mesenchymal transition (EMT) was inhibited by SPB
N-cadherin↓, decreased mesenchymal marker N-cadherin and increased epithelial marker E-cadherin.
E-cadherin↑,
TumVol↓, SPB induced remarkably tumor regression with decreased tumor volume
eff↑, phenylbutyrate improved the sensitivity of cisplatin for cell cycle arrest by inhibiting the FA/BRCA pathway in cancer cells.

2029- PB,    Phenylbutyric Acid: simple structure - multiple effects
- Review, Var, NA
NH3↓, enabling excretion of toxic ammonia, thus acting as ammonia scavenger
HDAC↓, histone deacetylase inhibiting
ChemChap↑, serving as chemical chaperone


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:


Core Metabolism/Glycolysis(tgid=4) ⓘ

glut↓, 1,   NH3↓, 2,  

Cell Death(tgid=5) ⓘ

Apoptosis?, 1,   Bcl-2↓, 1,   cl‑Casp3↑, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

ChemChap↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

HDAC↓, 1,  

Migration(tgid=13) ⓘ

E-cadherin↑, 1,   N-cadherin↓, 1,   TGF-β↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

eff↑, 1,   eff↝, 1,  

Functional Outcomes(tgid=23) ⓘ

TumVol↓, 1,  
Total Targets: 13

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

FFA/NEFA↝, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

KeyT↝, 1,   NH3↓, 3,  

Protein Folding & ER Stress(tgid=8) ⓘ

ER Stress↓, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

GH↑, 1,   HDAC↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

Dose↝, 1,  

Functional Outcomes(tgid=23) ⓘ

fatigue↓, 2,   hepatoP↑, 1,   Obesity↓, 1,   Sleep↑, 1,   toxicity↓, 2,  
Total Targets: 12

Scientific Paper Hit Count for: NH3, ammonia
3 Phenylbutyrate
2 L-ornithine
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#:218  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

 

Home Page