Early nerve ending rescue from oxidative damage and energy failure by l-carnitine as post-treatment in two neurotoxic models in rat: ... View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2009-06-30

AUTHORS

Diana Elinos-Calderón, Yolanda Robledo-Arratia, Verónica Pérez-De La Cruz, José Pedraza-Chaverrí, Syed F. Ali, Abel Santamaría

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 μM) were added to the isolated brain synaptosomes at different times (1, 3 and 6 h) after the incubation with toxins (100 μM 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/μl) or 3-NP (500 nmol/μl), 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. More... »

PAGES

287-296

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s00221-009-1913-3

DOI

http://dx.doi.org/10.1007/s00221-009-1913-3

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1046111332

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/19565224


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103 ongoing oxidative damage
104 oxidative damage
105 peroxidation
106 precursors
107 preservation
108 primary need
109 process
110 protection
111 purpose
112 quinolinic acid
113 rats
114 recovery
115 reductive capacity
116 rescue
117 results
118 significant amelioration
119 stage
120 striatal synaptosomes
121 study
122 synaptosomes
123 system
124 time
125 time of exposure
126 toxic events
127 toxic insults
128 toxic models
129 toxicity
130 toxin
131 variation
132 vivo conditions
133 vivo purposes
134 work
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