Citric acid-13C6

Citric acid-13C6 is the 13C-labeled Citric acid (HY-N1428) . Citric acid is a natural preservative and food tartness enhancer. Citric acid induces apoptosis and cell cycle arrest at G2/M phase and S phase in HaCaT cells. Citric acid cause oxidative damage of the liver by means of the decrease of antioxidative enzyme activities. Citric acid is also an acidulant, emulsifier, sequestrant and buffering agent widely used across many industries[1][2][3][4].

Product Specifications

CAS Number

[287389-42-8]

UNSPSC

12352211

Hazard Statement

H319, H335

Target

Apoptosis; Bacterial; Endogenous Metabolite; Isotope-Labeled Compounds

Type

Isotope-Labeled Compounds

Related Pathways

Anti-infection; Apoptosis; Metabolic Enzyme/Protease; Others

Field of Research

Cancer; Infection; Metabolic Disease; Inflammation/Immunology; Cardiovascular Disease

Assay Protocol

https://www.medchemexpress.com/citric-acid-13c6.html

Purity

99.90

Solubility

DMSO : 100mg/mL (ultrasonic) |H2O : 100mg/mL (ultrasonic)

Smiles

O[13C]([13CH2][13C]([13C](O)=O)(O)[13CH2][13C](O)=O)=O

Molecular Formula

13C6H8O7

Molecular Weight

198.08

Precautions

H319, H335

References & Citations

[1]Russak EM, et al. Impact of Deuterium Substitution on the Pharmacokinetics of Pharmaceuticals. Ann Pharmacother. 2019;53 (2) :211-216. |[2]Ying TH, et al. Citric acid induces cell-cycle arrest and apoptosis of human immortalized keratinocyte cell line (HaCaT) via caspase- and mitochondrial-dependent signaling pathways. Anticancer Res. 2013 Oct;33 (10) :4411-20.|[3]Abdel-Salam OM, et al. Citric acid effects on brain and liver oxidative stress in lipopolysaccharide-treated mice. J Med Food. 2014 May;17 (5) :588-98.|[4]Lacour B, et al. Stimulation by citric acid of calcium and phosphorus bioavailability in rats fed a calcium-rich diet. Miner Electrolyte Metab. 1997;23 (2) :79-87.|[5]Nagai R, et al. Citric acid inhibits development of cataracts, proteinuria and ketosis in streptozotocin (type 1) diabetic rats. Biochem Biophys Res Commun. 2010 Feb 26;393 (1) :118-22.