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Early nerve ending rescue from oxidative damage and energy failure by L: -carnitine as post-treatment in two neurotoxic models in rat: recovery of antioxidant and reductive capacities.
Exp Brain Res. 2009 Aug; 197(3):287-96.EB

Abstract

Cell rescue is a primary need during acute and chronic insults to the central nervous system. Functional preservation during the early stages of toxicity in a given degenerative event may represent a significant amelioration of detrimental processes linked to neuronal cell loss. Excitotoxicity and depleted cellular energy are toxic events leading to cell death in several neurodegenerative disorders. In this work, the effects of the well-known antioxidant and energy precursor, L: -carnitine (L: -CAR), were tested as a post-treatment in two neurotoxic models under in vitro and in vivo conditions. The experimental models tested included: (1) a typical excitotoxic and pro-oxidant inducer, quinolinic acid (QUIN); and (2) a mitochondrial energy inhibitor, 3-nitropropionic acid (3-NP). For in vitro studies, increasing concentrations of L: -CAR (10-1,000 microM) were added to the isolated brain synaptosomes at different times (1, 3 and 6 h) after the incubation with toxins (100 microM QUIN and 1 mM 3-NP), and 30 min later, lipid peroxidation (LP) and mitochondrial dysfunction (MD) were evaluated. For in vivo purposes, L: -CAR (100 mg/kg, i.p.) was given to rats either as a single administration 120 min after the intrastriatal infusion of QUIN (240 nmol/microl) or 3-NP (500 nmol/microl), or for 7 consecutive days (starting 120 min post-lesion). LP and MD were evaluated 4 h and 7 days post-lesions in isolated striatal synaptosomes. Our results show that, despite some variations depending on the toxic model tested, the time of exposure, or the biomarker evaluated, nerve ending protection can be mostly achieved by L: -CAR within the first hours after the toxic insults started, suggesting that targeting the ongoing oxidative damage and/or energy depletion during the first stages of neurotoxic events is essential to rescue nerve endings.

Authors+Show Affiliations

Laboratorio de Aminoácidos Excitadores, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, Insurgentes Sur 3877, C.P 14269, Mexico D.F., Mexico.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

19565224

Citation

Elinos-Calderón, Diana, et al. "Early Nerve Ending Rescue From Oxidative Damage and Energy Failure By L: -carnitine as Post-treatment in Two Neurotoxic Models in Rat: Recovery of Antioxidant and Reductive Capacities." Experimental Brain Research, vol. 197, no. 3, 2009, pp. 287-96.
Elinos-Calderón D, Robledo-Arratia Y, Pérez-De La Cruz V, et al. Early nerve ending rescue from oxidative damage and energy failure by L: -carnitine as post-treatment in two neurotoxic models in rat: recovery of antioxidant and reductive capacities. Exp Brain Res. 2009;197(3):287-96.
Elinos-Calderón, D., Robledo-Arratia, Y., Pérez-De La Cruz, V., Pedraza-Chaverrí, J., Ali, S. F., & Santamaría, A. (2009). Early nerve ending rescue from oxidative damage and energy failure by L: -carnitine as post-treatment in two neurotoxic models in rat: recovery of antioxidant and reductive capacities. Experimental Brain Research, 197(3), 287-96. https://doi.org/10.1007/s00221-009-1913-3
Elinos-Calderón D, et al. Early Nerve Ending Rescue From Oxidative Damage and Energy Failure By L: -carnitine as Post-treatment in Two Neurotoxic Models in Rat: Recovery of Antioxidant and Reductive Capacities. Exp Brain Res. 2009;197(3):287-96. PubMed PMID: 19565224.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Early nerve ending rescue from oxidative damage and energy failure by L: -carnitine as post-treatment in two neurotoxic models in rat: recovery of antioxidant and reductive capacities. AU - Elinos-Calderón,Diana, AU - Robledo-Arratia,Yolanda, AU - Pérez-De La Cruz,Verónica, AU - Pedraza-Chaverrí,José, AU - Ali,Syed F, AU - Santamaría,Abel, Y1 - 2009/06/30/ PY - 2009/04/24/received PY - 2009/06/15/accepted PY - 2009/7/1/entrez PY - 2009/7/1/pubmed PY - 2009/11/17/medline SP - 287 EP - 96 JF - Experimental brain research JO - Exp Brain Res VL - 197 IS - 3 N2 - Cell rescue is a primary need during acute and chronic insults to the central nervous system. Functional preservation during the early stages of toxicity in a given degenerative event may represent a significant amelioration of detrimental processes linked to neuronal cell loss. Excitotoxicity and depleted cellular energy are toxic events leading to cell death in several neurodegenerative disorders. In this work, the effects of the well-known antioxidant and energy precursor, L: -carnitine (L: -CAR), were tested as a post-treatment in two neurotoxic models under in vitro and in vivo conditions. The experimental models tested included: (1) a typical excitotoxic and pro-oxidant inducer, quinolinic acid (QUIN); and (2) a mitochondrial energy inhibitor, 3-nitropropionic acid (3-NP). For in vitro studies, increasing concentrations of L: -CAR (10-1,000 microM) were added to the isolated brain synaptosomes at different times (1, 3 and 6 h) after the incubation with toxins (100 microM QUIN and 1 mM 3-NP), and 30 min later, lipid peroxidation (LP) and mitochondrial dysfunction (MD) were evaluated. For in vivo purposes, L: -CAR (100 mg/kg, i.p.) was given to rats either as a single administration 120 min after the intrastriatal infusion of QUIN (240 nmol/microl) or 3-NP (500 nmol/microl), or for 7 consecutive days (starting 120 min post-lesion). LP and MD were evaluated 4 h and 7 days post-lesions in isolated striatal synaptosomes. Our results show that, despite some variations depending on the toxic model tested, the time of exposure, or the biomarker evaluated, nerve ending protection can be mostly achieved by L: -CAR within the first hours after the toxic insults started, suggesting that targeting the ongoing oxidative damage and/or energy depletion during the first stages of neurotoxic events is essential to rescue nerve endings. SN - 1432-1106 UR - https://www.unboundmedicine.com/medline/citation/19565224/Early_nerve_ending_rescue_from_oxidative_damage_and_energy_failure_by_L:__carnitine_as_post_treatment_in_two_neurotoxic_models_in_rat:_recovery_of_antioxidant_and_reductive_capacities_ L2 - https://dx.doi.org/10.1007/s00221-009-1913-3 DB - PRIME DP - Unbound Medicine ER -