3-Nitropropanoic acid
CAS No. : 504-88-1
(Synonyms: β-Nitropropionic acid; Bovinocidin)
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| Cat. No. : | HY-W012875 |
| M.Wt: | 119.08 |
| Formula: | C3H5NO4 |
| Purity: | >98 % |
| Solubility: | DMSO : 125 mg/mL (ultrasonic);H2O : 100 mg/mL (ultrasonic) |
3-Nitropropanoic acid (β-Nitropropionic acid) is an irreversible and orally active inhibitor of succinate dehydrogenase. 3-Nitropropanoic acid exhibits potent antimycobacterial activity with a MIC value of 3.3 μM. 3-Nitropropanoic acid can induce cell apoptosis[1][2].
IC50 & Target:succinate dehydrogenase[1]
In Vitro:3-Nitropropanoic acid (5 mM, 3 h) induces autophagy and disrupts mitochondrial morphology in SH-SY5Y cells[3].
3-Nitropropanoic acid (5 mM, 24 h) induces oxidative stress and apoptosis of granulosa cells in geese[4].
3-Nitropropanoic acid (0-15 mM, 48 h) induces cell death in cultured rat hippocampal neurons[5].
In Vivo:3-Nitropropanoic acid (20 mg/kg, i.p., BW/day for 4 days) induces oxidative stress, and increases lipid peroxidation in brain regions of the Wistar rat[6].
3-Nitropropanoic acid (100-200 mg/kg, i.p.) evokes seizures in mice[7].
Note:
Please do not refer to only one article to determine the experimental conditions. It is recommended to determine the optimal experimental conditions (animal strain, age, dosage, frequency and cycle, detection time and indicators, etc.) through preliminary experiments before the formal experiment.
3-Nitropropionic acid (20 mg/kg, i.p., once daily for 4 days) induces neural oxidative stress and mitochondrial dysfunction, evidenced by increased protein carbonyls, lipid peroxidation products, and decreased succinate dehydrogenase activity in the striatum and corte[6].
3-Nitropropionic acid (5-10 mg/kg, i.p., once daily for 14 days) increases succinate levels in all neuroanatomical regions, decreases taurine and GABA in the majority of brain regions, whereas altered lipid profiles were observed only in the globus pallidus and dorsal striatum[8].
3-Nitropropionic acid (10 mg/kg, i.p., every 4 days, total 4 times or more) exhibits hyperactivity, reaching a plateau after the third injection day 12 , then showing hypoactivity from the fourth injection day 16 onwards[9].
3-Nitropropionic acid causes spatial learning deficits, motor abnormalities, reduction in striatal area, enlargement of lateral ventricles, and striatal cell loss[10].
Administration: 3-Nitropropanoic acid 20 mg/kg • i.p. • once daily, total 4 days;
2. Rats: Sprague Dawley rats • male • 16-week-old
Administration: 3-Nitropropanoic acid 5.0 and 10.0 mg/kg • i.p. • once daily, total 14 days (Due to behavioral perturbations, the high dose (10 mg/kg) animals received a reduced dose of 7.5 mg/kg from day three onwards);
3. Rats: Sprague Dawley rats • male • 8-week-old
Administration: 3-Nitropropanoic acid 10 mg/kg • i.p. • every 4 days, total 4 times or more;
4. Rats: Sprague Dawley rats • male • 400-450 g
Administration: 3-Nitropropanoic acid 750 nmol/side (in 1 µL PBS) • bilateral intrastriatal injection (AP = + 1.5 mm; ML = ± 2.5 mm; DV = - 4.5 mm) • single dose
(2) The duration of a single injection into each striatum should be strictly controlled to be no less than 2 minutes. After injection, the needle should be left in place for 5 minutes before being slowly withdrawn. This procedure aims to prevent backflow of the medication along the injection path and ensure local deposition of the toxin in the target area.
Histology analysis: striatal cavitation, selective loss of medium spiny neurons, and reactive gliosis, lateral ventricle enlargement.
Behavioral analysis:hyperactivity (early-stage), hypoactivity (late-stage).
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