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Turski WA, Urbańska E, Sieklucka M, et al. Quinolinate-like neurotoxicity produced by aminooxyacetic acid in rat striatum. Amino Acids. 1992;2(3):245-53doi: 10.1007/BF00805946.
Turski, W. A., Urbańska, E., Sieklucka, M., & Ikonomidou, C. (1992). Quinolinate-like neurotoxicity produced by aminooxyacetic acid in rat striatum. Amino acids, 2(3), 245-53. https://doi.org/10.1007/BF00805946
Turski, W A, et al. "Quinolinate-like neurotoxicity produced by aminooxyacetic acid in rat striatum." Amino acids vol. 2,3 (1992): 245-53. doi: https://doi.org/10.1007/BF00805946
Turski WA, Urbańska E, Sieklucka M, Ikonomidou C. Quinolinate-like neurotoxicity produced by aminooxyacetic acid in rat striatum. Amino Acids. 1992 Oct;2(3):245-53. doi: 10.1007/BF00805946. PMID: 24192903.
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Amino Acids. 1992 Oct;2(3):245-53. doi: 10.1007/BF00805946.

Quinolinate-like neurotoxicity produced by aminooxyacetic acid in rat striatum.

Amino acids

W A Turski, E Urbańska, M Sieklucka, C Ikonomidou

Affiliations

  1. Department of Pharmacology, Medical School, Jaczewskiego 8, PL-20-090, Lublin, Poland.

PMID: 24192903 DOI: 10.1007/BF00805946

Abstract

The endogenous tryptophan metabolite quinolinic acid elicits in rodent brain a pattern of neuronal degeneration which resembles that caused by L-glutamate. Its qualities as a neurotoxic agent raised the hypothesis that quinolinic acid might be involved in the pathogenesis of human neurodegenerative disorders. Kynurenic acid, another endogenous tryptophan metabolite and preferential N-methyl-D-aspartate (NMDA) antagonist, has been shown to block quinolinic acid neurotoxicity. Here we report that microinjections of aminooxyacetic acid (AOAA), an inhibitor of kynurenine transaminase and of other pyridoxal phosphate-dependent enzymes, into the rat striatum produce neuronal damage resembling that caused by quinolinic acid. AOAA-induced striatal lesions can be prevented by kynurenic acid and the selective NMDA antagonist 2-amino-7-phosphonoheptanoic acid. These results suggest that AOAA produces excitotoxic lesions by depleting brain concentrations of kynurenic acid (inhibition of synthetic enzyme) or due to impairment of intracellular energy metabolism (depletion of cell energy resources). The concept of deficient neuroprotection due to metabolic defects might help to clarify the pathogenesis of human neurodegenerative disorders and to develop strategies that may be useful in their treatment.

References

  1. J Neurochem. 1958 Oct;3(1):8-18 - PubMed
  2. Neurosci Lett. 1984 Aug 10;48(3):273-8 - PubMed
  3. J Pharmacol Exp Ther. 1990 Jun;253(3):1285-92 - PubMed
  4. J Neurochem. 1990 Dec;55(6):2142-5 - PubMed
  5. Nature. 1986 May 8-14;321(6066):168-71 - PubMed
  6. Neuroscience. 1985 Feb;14(2):417-26 - PubMed
  7. Brain Res. 1988 Aug 30;459(1):200-3 - PubMed
  8. Nature. 1976 Oct 7;263(5577):517-9 - PubMed
  9. Nature. 1991 Jan 31;349(6308):414-8 - PubMed
  10. Neurosci Lett. 1986 Mar 28;65(1):65-71 - PubMed
  11. J Biol Chem. 1949 Dec;181(2):667-75 - PubMed
  12. J Biol Chem. 1951 Nov;193(1):265-75 - PubMed
  13. Anal Biochem. 1978 Jun 15;87(1):206-10 - PubMed
  14. J Neurosci. 1989 Aug;9(8):2809-18 - PubMed
  15. Brain Res. 1988 Jun 7;451(1-2):205-12 - PubMed
  16. Science. 1983 Jan 21;219(4582):316-8 - PubMed
  17. Life Sci. 1984 Jul 2;35(1):19-32 - PubMed
  18. Neurology. 1990 Aug;40(8):1231-4 - PubMed
  19. Exp Brain Res. 1971;14(1):61-76 - PubMed
  20. Brain Res. 1983 Aug 22;273(1):170-4 - PubMed
  21. Brain Res. 1988 Jun 28;454(1-2):164-9 - PubMed
  22. Nature. 1970 Aug 8;227(5258):609-11 - PubMed
  23. Toxicol Appl Pharmacol. 1964 Jul;6:388-95 - PubMed
  24. Brain Res. 1967 Apr;4(4):369-74 - PubMed
  25. J Neurochem. 1989 May;52(5):1629-36 - PubMed
  26. Prog Neuropsychopharmacol. 1977;1(1-2):13-30 - PubMed
  27. Nature. 1976 Sep 16;263(5574):244-6 - PubMed

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