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Neuroprotective effect of taurine in 3-nitropropionic acid-induced experimental animal model of Huntington's disease phenotype.
Pharmacol Biochem Behav. 2005 Nov; 82(3):574-82.PB

Abstract

An experimental animal model of Huntington's disease (HD) phenotype was induced using the mycotoxin 3-nitropropionic acid (3-NP) and was well characterized behaviorally, neurochemically, morphometrically and histologically. Administration of 3-NP caused a reduction in prepulse inhibition (PPI) of acoustic startle response, locomotor hyper- and/or hypoactivity, bilateral striatal lesions, brain oxidative stress, and decreased striatal gamma-aminobutyric acid (GABA) levels. Taurine is a semi-essential beta-amino acid that was demonstrated to have both antioxidant and GABA-A agonistic activity. In this study, treatment with taurine (200 mg/kg daily for 3 days) prior to 3-NP administration reversed both reduced PPI response and locomotor hypoactivity caused by 3-NP injection. Taurine pretreatment also caused about 2-fold increase in GABA concentration compared to 3-NP-treated animals. In addition, taurine demonstrated antioxidant activity against oxidative stress induced by 3-NP administration as evidenced by the reduced striatal malondialdehyde (MDA) and elevated striatal glutathione (GSH) levels. Histochemical examination of striatal tissue showed that prior administration of taurine ahead of 3-NP challenge significantly increased succinate dehydrogenase (SDH) activity compared to 3-NP-treated animals. Histopathological examination further affirmed the neuroprotective effect of taurine in 3-NP-induced HD in rats. Taken together, one may conclude that taurine has neuroprotective role in the current HD paradigm due, at least partly, to its indirect antioxidant effect and GABA agonistic action.

Authors+Show Affiliations

Tadros MG
Department of Pharmacology and Toxicology, Faculty of Pharmacy, Ain Shams University, Cairo, Egypt.
Khalifa AE
No affiliation info available
Abdel-Naim AB
No affiliation info available
Arafa HM
No affiliation info available

MeSH

AnimalsCorpus StriatumDisease Models, AnimalHuntington DiseaseMaleMotor ActivityNeuroprotective AgentsNitro CompoundsOxidative StressPhenotypePropionatesRatsRats, WistarReflex, StartleTaurinegamma-Aminobutyric Acid

Pub Type(s)

Journal Article

Language

eng

PubMed ID

16337998

Citation

Tadros, Mariane G., et al. "Neuroprotective Effect of Taurine in 3-nitropropionic Acid-induced Experimental Animal Model of Huntington's Disease Phenotype." Pharmacology, Biochemistry, and Behavior, vol. 82, no. 3, 2005, pp. 574-82.
Tadros MG, Khalifa AE, Abdel-Naim AB, et al. Neuroprotective effect of taurine in 3-nitropropionic acid-induced experimental animal model of Huntington's disease phenotype. Pharmacol Biochem Behav. 2005;82(3):574-82.
Tadros, M. G., Khalifa, A. E., Abdel-Naim, A. B., & Arafa, H. M. (2005). Neuroprotective effect of taurine in 3-nitropropionic acid-induced experimental animal model of Huntington's disease phenotype. Pharmacology, Biochemistry, and Behavior, 82(3), 574-82.
Tadros MG, et al. Neuroprotective Effect of Taurine in 3-nitropropionic Acid-induced Experimental Animal Model of Huntington's Disease Phenotype. Pharmacol Biochem Behav. 2005;82(3):574-82. PubMed PMID: 16337998.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Neuroprotective effect of taurine in 3-nitropropionic acid-induced experimental animal model of Huntington's disease phenotype. AU - Tadros,Mariane G, AU - Khalifa,Amani E, AU - Abdel-Naim,Ashraf B, AU - Arafa,Hossam M M, Y1 - 2005/12/09/ PY - 2005/05/16/received PY - 2005/10/09/revised PY - 2005/10/26/accepted PY - 2005/12/13/pubmed PY - 2006/3/3/medline PY - 2005/12/13/entrez SP - 574 EP - 82 JF - Pharmacology, biochemistry, and behavior JO - Pharmacol Biochem Behav VL - 82 IS - 3 N2 - An experimental animal model of Huntington's disease (HD) phenotype was induced using the mycotoxin 3-nitropropionic acid (3-NP) and was well characterized behaviorally, neurochemically, morphometrically and histologically. Administration of 3-NP caused a reduction in prepulse inhibition (PPI) of acoustic startle response, locomotor hyper- and/or hypoactivity, bilateral striatal lesions, brain oxidative stress, and decreased striatal gamma-aminobutyric acid (GABA) levels. Taurine is a semi-essential beta-amino acid that was demonstrated to have both antioxidant and GABA-A agonistic activity. In this study, treatment with taurine (200 mg/kg daily for 3 days) prior to 3-NP administration reversed both reduced PPI response and locomotor hypoactivity caused by 3-NP injection. Taurine pretreatment also caused about 2-fold increase in GABA concentration compared to 3-NP-treated animals. In addition, taurine demonstrated antioxidant activity against oxidative stress induced by 3-NP administration as evidenced by the reduced striatal malondialdehyde (MDA) and elevated striatal glutathione (GSH) levels. Histochemical examination of striatal tissue showed that prior administration of taurine ahead of 3-NP challenge significantly increased succinate dehydrogenase (SDH) activity compared to 3-NP-treated animals. Histopathological examination further affirmed the neuroprotective effect of taurine in 3-NP-induced HD in rats. Taken together, one may conclude that taurine has neuroprotective role in the current HD paradigm due, at least partly, to its indirect antioxidant effect and GABA agonistic action. SN - 0091-3057 UR - https://www.unboundmedicine.com/medline/citation/16337998/Neuroprotective_effect_of_taurine_in_3_nitropropionic_acid_induced_experimental_animal_model_of_Huntington's_disease_phenotype_ DB - PRIME DP - Unbound Medicine ER -