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MedChemExpressModel 3-Methylglutaconic acid -5746-90-7

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3-Methylglutaconic acid is the major metabolites accumulating in 3-Methylglutaconic aciduria (MGTA). 3-Methylglutaconic acid can induce lipid oxidative damage and protein oxidative. 3-Methylglutaconic acid decreases the non-enzymatic antioxidant defenses in cerebral cortex supernatants to elicit oxidative stress in the cerebral cortex. 3-Methylglutaconic acid can be used for brain damage disease research[1].
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3-Methylglutaconic acid

MCE China:3-Methylglutaconic acid

Brand:MedChemExpress (MCE)

Cat. No.HY-139427

CAS:5746-90-7

Synonyms:β-Methylglutaconic acid

Purity:99.60%

Storage:Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month

Shipping:Room temperature in continental US; may vary elsewhere.

Description:3-Methylglutaconic acid is the major metabolites accumulating in 3-Methylglutaconic aciduria (MGTA). 3-Methylglutaconic acid can induce lipid oxidative damage and protein oxidative. 3-Methylglutaconic acid decreases the non-enzymatic antioxidant defenses in cerebral cortex supernatants to elicit oxidative stress in the cerebral cortex. 3-Methylglutaconic acid can be used for brain damage disease research.

In Vitro:3-Methylglutaconic acid (0.1-5.0 mM, 1 h) induces lipid oxidative damage and antioxidants (TRO, MEL and SOD plus CAT) prevent the lipid peroxidation at higher doses of 5 mM in rat cerebral cortex supernatants[1]. 3-Methylglutaconic acid (0.1-5.0 mM, 1 h) induces protein oxidative damage and diminishes non-enzymatic antioxidant defenses in rat cerebral cortex supernatants[1].

In Vivo:Animal Model: Male Sprague-Dawley rats and male Hartley guinea-pigs[2] Dosage: 0.16 mL/kg, 90 min Administration: Intraperitoneal injection (i.p.) Result: Increased initial blood pressure and heart rate in rats followed by vagal bradycardia and hypotension (rat) Developed three patterns of cardiovascular changes (Type 1: a period of sympathetically-mediated hypertension and tachycardia followed by vagal bradycardia; Type 2: Increased arterial pressure and heart rate, but no vagal activation; Type 3: exhibited no significant cardiovascular changes(Guinea-pigs). Animal Model: Male Wistar rats[3] Dosage: 45mg/kg for single dose, 4days Administration: Intraperitoneal injection (i.p.) Result: Decreased in NR2B expression on the whole cerebellum tissue and Purkinje cells. Molecular Weight 144.13

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References:

[1]. Guilhian Leipnitz, et al. Induction of oxidative stress by the metabolites accumulating in 3-methylglutaconic aciduria in cerebral cortex of young rats. Life Sci. 2008 Mar 12;82(11-12):652-62.  [Content Brief]

[2]. N L Alsip, et al. Cardiovascular effects of 3-mercaptopropionic acid and levels of GABA in regions of the brain of guinea-pigs. Neuropharmacology. 1984 Mar;23(3):349-57.  [Content Brief]

[3]. E Girardi, et al. 3-mercaptopropionic acid-induced seizures decrease NR2B expression in Purkinje cells: cyclopentyladenosine effect. Cell Mol Neurobiol. 2010 Oct;30(7):985-90.  [Content Brief]

[4]. Leipnitz G, et al. Induction of oxidative stress by the metabolites accumulating in 3-methylglutaconic aciduria in cerebral cortex of young rats. Life Sci. 2008 Mar 12;82(11-12):652-62.  [Content Brief]

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