107-22-2
Chemical Structure
Glyoxal (40% w/w in water)
- CAS. Nr.: 107-22-2
- Formula:C2H2O2
- Molecular Weight:58.04
IUPAC Name: oxalaldehyde
InChIKey: LEQAOMBKQFMDFZ-UHFFFAOYSA-N
SMILES: O=CC=O
Biological Activity: Glyoxal (40% w/w in water) is an α-oxoaldehyde that inhibits Aldose Reductase, Glutathione Reductase, and NADPH synthase. Glyoxal (40% w/w in water) exhibits cytotoxicity, triggers oxidative stress, induces ROS accumulation, lipid peroxidation, mitochondrial membrane potential collapse, DNA damage, apoptosis, and massive production of advanced glycation end products (AGEs). Glyoxal (40% w/w in water) depletes glutathione and activates MAPK phosphorylation. It has lower toxicity as a fixative than paraformaldehyde (PFA) and serves as a precursor for the synthesis of oxalates and dietary carcinogens. Glyoxal (40% w/w in water) is suitable for research related to calcium oxalate kidney stones, diabetes, atherosclerosis, cardiovascular diseases, retinopathy, and cataracts[1][2][3][4][5][6][7].
| Art. -Nr. | Produktname | Reinheit | Beschreibung | Pricing | |||||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
|
|
Glyoxal (40% w/w in water) | Glyoxal (40% w/w in water) is an α-oxoaldehyde that inhibits Aldose Reductase, Glutathione Reductase, and NADPH synthase. Glyoxal (40% w/w in water) exhibits cytotoxicity, triggers oxidative stress, induces ROS accumulation, lipid peroxidation, mitochondrial membrane potential collapse, DNA damage, apoptosis, and massive production of advanced glycation end products (AGEs). Glyoxal (40% w/w in water) depletes glutathione and activates MAPK phosphorylation. It has lower toxicity as a fixative than paraformaldehyde (PFA) and serves as a precursor for the synthesis of oxalates and dietary carcinogens. Glyoxal (40% w/w in water) is suitable for research related to calcium oxalate kidney stones, diabetes, atherosclerosis, cardiovascular diseases, retinopathy, and cataracts. | |||||||||||||||||||||
|
loading...
/
|
|||||||||||||||||||||||
- [1]. Lange JN, et al. Glyoxal formation and its role in endogenous oxalate synthesis. Advances in urology. 2012;2012:819202. [Content Brief]
- [2]. Shangari N, et al. The cytotoxic mechanism of glyoxal involves oxidative stress. Biochemical pharmacology. 2004 Oct 01;68(7):1433-42. [Content Brief]
- [3]. Richter KN, et al. Glyoxal as an alternative fixative to formaldehyde in immunostaining and super-resolution microscopy. The EMBO journal. 2018 Jan 04;37(1):139-159. [Content Brief]
- [4]. Zhang M, et al. Glyoxal in Foods: Formation, Metabolism, Health Hazards, and Its Control Strategies. Journal of agricultural and food chemistry. 2024 Feb 07;72(5):2434-2450. [Content Brief]
- [5]. Xie MZ, et al. Glyoxal damages human aortic endothelial cells by perturbing the glutathione, mitochondrial membrane potential, and mitogen-activated protein kinase pathways. BMC cardiovascular disorders. 2021 Dec 18;21(1):603. [Content Brief]
- [6]. Sliman SM, et al. Hyperglycemic oxoaldehyde, glyoxal, causes barrier dysfunction, cytoskeletal alterations, and inhibition of angiogenesis in vascular endothelial cells: aminoguanidine protection. Molecular and cellular biochemistry. 2010 Jan;333(1-2):9-26. [Content Brief]
- [7]. Reber F, et al. Alteration of the intracellular pH and apoptosis induction in a retinal cell line by the AGE-inducing agent glyoxal. Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie. 2002 Dec;240(12):1022-32. [Content Brief]
Keywords