Bioactivity | Citric acid-18O is 18O-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 causes renal toxicity in mice. |
Invitro | Stable heavy isotopes of hydrogen, carbon, and other elements have been incorporated into drug molecules, largely as tracers for quantitation during the drug development process. Deuteration has gained attention because of its potential to affect the pharmacokinetic and metabolic profiles of drugs[1]. MCE has not independently confirmed the accuracy of these methods. They are for reference only. 0 --> Citric acid-18O 相关抗体: |
In Vivo | Citric acid (120, 240, and 480 mg/kg; i.p.) significantly decreases GSH-Px activity and induces an increase in the MDA (malonyldialdehyde) levels in mouse liver[1]. Citric acid (120, 240, and 480 mg/kg; i.p.) induces apoptosis by increases caspase-3 activity in a dose-dependent manner in mouse hepatocytes[1].Citric acid (120, 240, and 480 mg/kg; i.p.; weekly for 3 weeks) causes renal toxicity in mice[2]. MCE has not independently confirmed the accuracy of these methods. They are for reference only. |
Formula | C6H8O618O |
Molar Mass | 194.12 |
Transport | Room temperature in continental US; may vary elsewhere. |
Storage | Please store the product under the recommended conditions in the Certificate of Analysis. |
Reference | [1]. Russak EM, et al. Impact of Deuterium Substitution on the Pharmacokinetics of Pharmaceuticals. Ann Pharmacother. 2019;53(2):211-216. [2]. Chen X, et al. Study on injury effect of food additive citric acid on liver tissue in mice. Cytotechnology. 2014 Mar;66(2):275-82. [3]. Chen X, Lv Q, Liu Y, Deng W. Effects of the food additive, citric acid, on kidney cells of mice. Biotech Histochem. 2015 Jan;90(1):38-44. [4]. 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. |