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Mitochondrial toxin 3-nitropropionic acid evokes seizures in mice.

Abstract
3-Nitropropionic acid, a potent inhibitor of succinate dehydrogenase which thus compromises cellular energy metabolism, evoked convulsions in mice in a dose-dependent manner. CD50 for clonic seizures was 158.5 (144.1-174.3) mg/kg. Tonic seizures were not observed. Broad-spectrum anticonvulsants, namely diazepam, phenobarbital and valproate, prevented the occurrence of 3-nitropropionic acid-induced seizures with ED50 of 4.9 (3.1-7.6), 33.1 (17.9-61.0) and 389.7 (351.2-432.3) mg/kg, respectively. Diphenylhydantoin-like drugs (diphenylhydantoin, and carbamazepine), anti-absence drugs (trimethadione and ethosuximide) and acetazolamide were ineffective. The characteristics of 3-nitropropionic acid-induced seizures resembled those of convulsions evoked by another mitochondrial toxin, aminooxyacetic acid.
AuthorsE M Urbanska, P Blaszczak, T Saran, Z Kleinrok, W A Turski
JournalEuropean journal of pharmacology (Eur J Pharmacol) Vol. 359 Issue 1 Pg. 55-8 (Oct 16 1998) ISSN: 0014-2999 [Print] Netherlands
PMID9831293 (Publication Type: Journal Article)
Chemical References
  • Anticonvulsants
  • Neurotoxins
  • Nitro Compounds
  • Propionates
  • 3-nitropropionic acid
Topics
  • Animals
  • Anticonvulsants (therapeutic use)
  • Dose-Response Relationship, Drug
  • Male
  • Mice
  • Mitochondria (drug effects)
  • Neurotoxins (pharmacology)
  • Nitro Compounds
  • Propionates (pharmacology)
  • Seizures (chemically induced, drug therapy)

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