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S-Allylcysteine, a garlic-derived antioxidant, ameliorates quinolinic acid-induced neurotoxicity and oxidative damage in rats.

Abstract

Excitotoxicity elicited by overactivation of N-methyl-D-aspartate receptors is a well-known characteristic of quinolinic acid-induced neurotoxicity. However, since many experimental evidences suggest that the actions of quinolinic acid also involve reactive oxygen species formation and oxidative stress as major features of its pattern of toxicity, the use of antioxidants as experimental tools against the deleterious effects evoked by this neurotoxin becomes more relevant. In this work, we investigated the effect of a garlic-derived compound and well-characterized free radical scavenger, S-allylcysteine, on quinolinic acid-induced striatal neurotoxicity and oxidative damage. For this purpose, rats were administered S-allylcysteine (150, 300 or 450 mg/kg, i.p.) 30 min before a single striatal infusion of 1 microl of quinolinic acid (240 nmol). The lower dose (150 mg/kg) of S-allylcysteine resulted effective to prevent only the quinolinate-induced lipid peroxidation (P < 0.05), whereas the systemic administration of 300 mg/kg of this compound to rats decreased effectively the quinolinic acid-induced oxidative injury measured as striatal reactive oxygen species formation (P < 0.01) and lipid peroxidation (P < 0.05). S-Allylcysteine (300 mg/kg) also prevented the striatal decrease of copper/zinc-superoxide dismutase activity (P < 0.05) produced by quinolinate. In addition, S-allylcysteine, at the same dose tested, was able to reduce the quinolinic acid-induced neurotoxicity evaluated as circling behavior (P < 0.01) and striatal morphologic alterations. In summary, S-allylcysteine ameliorates the in vivo quinolinate striatal toxicity by a mechanism related to its ability to: (a) scavenge free radicals; (b) decrease oxidative stress; and (c) preserve the striatal activity of Cu,Zn-superoxide dismutase (Cu,Zn-SOD). This antioxidant effect seems to be responsible for the preservation of the morphological and functional integrity of the striatum.

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  • Authors+Show Affiliations

    ,

    Departamento de Neuroquímica, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, México D.F. 14269, Mexico.

    , , , , , , , , ,

    Source

    Neurochemistry international 45:8 2004 Dec pg 1175-83

    MeSH

    Animals
    Antioxidants
    Behavior, Animal
    Blotting, Western
    Body Weight
    Cysteine
    Garlic
    Glutathione Peroxidase
    Lipid Peroxidation
    Male
    Neostriatum
    Neurotoxicity Syndromes
    Oxidative Stress
    Quinolinic Acid
    RNA, Messenger
    Rats
    Rats, Wistar
    Reactive Oxygen Species
    Reverse Transcriptase Polymerase Chain Reaction
    Superoxide Dismutase

    Pub Type(s)

    Journal Article
    Research Support, Non-U.S. Gov't

    Language

    eng

    PubMed ID

    15380627

    Citation

    Pérez-Severiano, Francisca, et al. "S-Allylcysteine, a Garlic-derived Antioxidant, Ameliorates Quinolinic Acid-induced Neurotoxicity and Oxidative Damage in Rats." Neurochemistry International, vol. 45, no. 8, 2004, pp. 1175-83.
    Pérez-Severiano F, Rodríguez-Pérez M, Pedraza-Chaverrí J, et al. S-Allylcysteine, a garlic-derived antioxidant, ameliorates quinolinic acid-induced neurotoxicity and oxidative damage in rats. Neurochem Int. 2004;45(8):1175-83.
    Pérez-Severiano, F., Rodríguez-Pérez, M., Pedraza-Chaverrí, J., Maldonado, P. D., Medina-Campos, O. N., Ortíz-Plata, A., ... Santamaría, A. (2004). S-Allylcysteine, a garlic-derived antioxidant, ameliorates quinolinic acid-induced neurotoxicity and oxidative damage in rats. Neurochemistry International, 45(8), pp. 1175-83.
    Pérez-Severiano F, et al. S-Allylcysteine, a Garlic-derived Antioxidant, Ameliorates Quinolinic Acid-induced Neurotoxicity and Oxidative Damage in Rats. Neurochem Int. 2004;45(8):1175-83. PubMed PMID: 15380627.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - S-Allylcysteine, a garlic-derived antioxidant, ameliorates quinolinic acid-induced neurotoxicity and oxidative damage in rats. AU - Pérez-Severiano,Francisca, AU - Rodríguez-Pérez,Mayra, AU - Pedraza-Chaverrí,José, AU - Maldonado,Perla D, AU - Medina-Campos,Omar N, AU - Ortíz-Plata,Alma, AU - Sánchez-García,Aurora, AU - Villeda-Hernández,Juana, AU - Galván-Arzate,Sonia, AU - Aguilera,Penélope, AU - Santamaría,Abel, PY - 2004/03/31/received PY - 2004/06/21/accepted PY - 2004/9/24/pubmed PY - 2004/12/21/medline PY - 2004/9/24/entrez SP - 1175 EP - 83 JF - Neurochemistry international JO - Neurochem. Int. VL - 45 IS - 8 N2 - Excitotoxicity elicited by overactivation of N-methyl-D-aspartate receptors is a well-known characteristic of quinolinic acid-induced neurotoxicity. However, since many experimental evidences suggest that the actions of quinolinic acid also involve reactive oxygen species formation and oxidative stress as major features of its pattern of toxicity, the use of antioxidants as experimental tools against the deleterious effects evoked by this neurotoxin becomes more relevant. In this work, we investigated the effect of a garlic-derived compound and well-characterized free radical scavenger, S-allylcysteine, on quinolinic acid-induced striatal neurotoxicity and oxidative damage. For this purpose, rats were administered S-allylcysteine (150, 300 or 450 mg/kg, i.p.) 30 min before a single striatal infusion of 1 microl of quinolinic acid (240 nmol). The lower dose (150 mg/kg) of S-allylcysteine resulted effective to prevent only the quinolinate-induced lipid peroxidation (P < 0.05), whereas the systemic administration of 300 mg/kg of this compound to rats decreased effectively the quinolinic acid-induced oxidative injury measured as striatal reactive oxygen species formation (P < 0.01) and lipid peroxidation (P < 0.05). S-Allylcysteine (300 mg/kg) also prevented the striatal decrease of copper/zinc-superoxide dismutase activity (P < 0.05) produced by quinolinate. In addition, S-allylcysteine, at the same dose tested, was able to reduce the quinolinic acid-induced neurotoxicity evaluated as circling behavior (P < 0.01) and striatal morphologic alterations. In summary, S-allylcysteine ameliorates the in vivo quinolinate striatal toxicity by a mechanism related to its ability to: (a) scavenge free radicals; (b) decrease oxidative stress; and (c) preserve the striatal activity of Cu,Zn-superoxide dismutase (Cu,Zn-SOD). This antioxidant effect seems to be responsible for the preservation of the morphological and functional integrity of the striatum. SN - 0197-0186 UR - https://www.unboundmedicine.com/medline/citation/15380627/S_Allylcysteine_a_garlic_derived_antioxidant_ameliorates_quinolinic_acid_induced_neurotoxicity_and_oxidative_damage_in_rats_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0197-0186(04)00127-5 DB - PRIME DP - Unbound Medicine ER -