3-Methylglutaconic acid, a primary metabolite accumulating in 3-Methylglutaconic aciduria (MGTA), induces lipid and protein oxidation, while diminishing non-enzymatic antioxidant defenses in cerebral cortex supernatants, thereby promoting oxidative stress in the cerebral cortex. This compound is utilized in research concerning brain damage diseases [1].

3-Methylglutaconic acid (0.1-5.0 mM, 1 hour) induces lipid peroxidation and protein oxidative damage in rat cerebral cortex supernatant, while antioxidants (TRO, MEL, and SOD plus CAT) at 5 mM prevent lipid peroxidation [1]. The compound also reduces non-enzymatic antioxidant defenses [1].

In animal models using male Sprague-Dawley rats and male Hartley guinea pigs [2], a 0.16 mL/kg intraperitoneal injection (i.p.) resulted in an initial increase in blood pressure and heart rate in rats, later giving way to vagal bradycardia and hypotension (rat). The compound elicited three distinct cardiovascular response patterns: Type 1—sympathetically-mediated hypertension and tachycardia succeeded by vagal bradycardia; Type 2—elevated arterial pressure and heart rate without vagal activation; Type 3—no notable cardiovascular change (guinea pigs). A separate study on male Wistar rats [3] demonstrated that a single i.p. dose of 45mg/kg administered over four days led to a reduction in NR2B expression in cerebellar tissue, including the Purkinje cells.