Antioxidant strategy to rescue synaptosomes from oxidative damage and energy failure in neurotoxic models in rats: protective role of S-allylcysteine View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2009-10-29

AUTHORS

Diana Elinos-Calderón, Yolanda Robledo-Arratia, Verónica Pérez-De La Cruz, Perla D. Maldonado, Sonia Galván-Arzate, José Pedraza-Chaverrí, Abel Santamaría

ABSTRACT

The functional preservation of nerve endings since the early stages of toxicity in a given damaging insult—either acute or chronic—by means of antioxidant and neuroprotective agents is a primary need to design therapeutic strategies for neurodegenerative disorders, with particular emphasis on those diseases with excitotoxic and depleted energy metabolism components. S-allylcysteine (SAC), a well-known antioxidant agent, was tested as a post-treatment in different in vitro and in vivo neurotoxic models. Quinolinic acid (QUIN) was used as a typical excitotoxic/pro-oxidant inducer, 3-nitropropionic acid (3-NP) was employed as a mitochondrial function inhibitor, and their combination (QUIN + 3-NP) was also evaluated in in vitro studies. For in vitro purposes, increasing concentrations of SAC (10–100 μM) were added to isolated brain synaptosomes at different times (1, 3 and 6 h) after the incubation with toxins (100 μM QUIN, 1 mM 3-NP or the combination of QUIN (21 μM) + 3-NP (166 μM). Thirty minutes later, lipid peroxidation (LP) and mitochondrial dysfunction (MD) were evaluated. For in vivo studies, SAC (100 mg/kg, i.p.) was given to QUIN- or 3-NP-striatally lesioned rats for 7 consecutive days (starting 120 min post-lesion). LP and MD were evaluated 7 days post-lesion in isolated striatal synaptosomes. Circling behavior was also assessed. Our results describe a differential pattern of protection achieved by SAC, mostly expressed in the 3-NP toxic model, in which nerve ending protection was found within the first hours (1 and 3) after the toxic insult started, supporting the concept that the ongoing oxidative damage and energy depletion can be treated during the first stages of neurotoxic events. More... »

PAGES

35

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s00702-009-0299-5

DOI

http://dx.doi.org/10.1007/s00702-009-0299-5

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1015201520

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/19866339


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47 combination
48 components
49 concentration
50 concentrations of SAC
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52 different times
53 disease
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55 early stages
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57 endings
58 energy metabolism components
59 excitotoxic
60 function inhibitors
61 functional preservation
62 incubation
63 inducer
64 inhibitors
65 insult
66 means
67 metabolism components
68 mitochondrial function inhibitor
69 model
70 need
71 nerve endings
72 neurodegenerative disorders
73 neuroprotective agents
74 neurotoxic models
75 particular emphasis
76 preservation
77 primary need
78 purpose
79 quinolinic acid
80 sac
81 stage
82 strategies
83 study
84 synaptosomes
85 therapeutic strategies
86 time
87 toxicity
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