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O7753

Sigma-Aldrich

Oxaloacetic acid

powder, BioReagent, suitable for cell culture, suitable for insect cell culture, ≥97% (HPLC)

Synonyme(s) :

2-Oxosuccinic acid, Ketosuccinic acid, Oxalacetic acid, Oxobutanedioic acid

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About This Item

Formule linéaire :
HOOCCH2COCOOH
Numéro CAS:
328-42-7
Poids moléculaire :
132.07
Numéro Beilstein :
1705475
Numéro CE :
206-329-8
Numéro MDL:
MFCD00002592
Code UNSPSC :
12352204
ID de substance PubChem :
24898047
Nomenclature NACRES :
NA.75

Source biologique

synthetic (organic)

Niveau de qualité

200

Gamme de produits

BioReagent

Pureté

≥97% (HPLC)

Forme

powder

Technique(s)

cell culture | insect: suitable
cell culture | mammalian: suitable

Solubilité

H2O: 100 mg/mL

Température de stockage

−20°C

Chaîne SMILES 

OC(=O)CC(=O)C(O)=O

InChI

1S/C4H4O5/c5-2(4(8)9)1-3(6)7/h1H2,(H,6,7)(H,8,9)

Clé InChI

KHPXUQMNIQBQEV-UHFFFAOYSA-N

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Catégories apparentées

Description générale

Oxaloacetic acid is a dicarboxylic acid that is present in every cell in the body. It is a metabolic intermediate of the tricarboxylic acid (TCA) cycle and gluconeogenesis.

Application

Oxaloacetic acid has been used to evaluate its effect on neuromuscular function and lifespan in amyotrophic lateral sclerosis (ALS) model superoxide dismutase 1 (SOD1) G93A mice. It has also been used as a supplement in Dulbecco′s modified Eagle′s medium (DMEM) to culture chicken fibroblast (DF-1) cells and chemically immortalized leghorn male hepatoma (LMH) cells for functional validation experiments.

Actions biochimiques/physiologiques

Oxaloacetic acid plays a vital role in central metabolism. It inhibits succinate dehydrogenase and is a key regulator of mitochondrial metabolism.

Produit(s) apparenté(s)

Réf. du produit
Description
Tarif

Pictogrammes

Exclamation mark
GHS07

Mention d'avertissement

Warning

Mentions de danger

H319

Classification des risques

Eye Irrit. 2

Code de la classe de stockage

11 - Combustible Solids

Classe de danger pour l'eau (WGK)

WGK 1

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable

Équipement de protection individuelle

Eyeshields, Faceshields, Gloves, type P3 (EN 143) respirator cartridges

Certificats d'analyse (COA)

Recherchez un Certificats d'analyse (COA) en saisissant le numéro de lot du produit. Les numéros de lot figurent sur l'étiquette du produit après les mots "Lot" ou "Batch".

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Consulter la Bibliothèque de documents

Randy J Giedt et al.
Free radical biology & medicine, 52(2), 348-356 (2011-11-22)
Ischemia (I)/reperfusion (RP)-induced endothelial cell (EC) injury is thought to be due to mitochondrial reactive oxygen species (mtROS) production. MtROS have been implicated in mitochondrial fission. We determined whether cultured EC exposure to simulated I/RP causes morphological changes in the
Randy Strong et al.
The journals of gerontology. Series A, Biological sciences and medical sciences, 68(1), 6-16 (2012-03-28)
The National Institute on Aging Interventions Testing Program (ITP) was established to evaluate agents that are hypothesized to increase life span and/or health span in genetically heterogeneous mice. Each compound is tested in parallel at three test sites. It is
Tonya N Zeczycki et al.
Biochemistry, 50(45), 9724-9737 (2011-10-01)
The catalytic mechanism of the MgATP-dependent carboxylation of biotin in the biotin carboxylase domain of pyruvate carboxylase from R. etli (RePC) is common to the biotin-dependent carboxylases. The current site-directed mutagenesis study has clarified the catalytic functions of several residues
L T Wong et al.
Pediatric research, 20(3), 274-279 (1986-03-01)
An infant with the acute neonatal form of pyruvate carboxylase deficiency (cross-reacting material negative) presented with severe intractable lactic acidosis within 4 h after birth. He also had hyperammonemia, hypercitrullinemia, and hyperlysinemia. Plasma glutamine was not elevated. He had a
Alexander Zlotnik et al.
Anesthesiology, 116(1), 73-83 (2011-12-02)
Decreasing blood glutamate concentrations after traumatic brain injury accelerates brain-to-blood glutamate efflux, leading to improved neurologic outcomes. The authors hypothesize that treatment with blood glutamate scavengers should reduce neuronal cell loss, whereas administration of glutamate should worsen outcomes. The authors
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