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Sulforaphane prevents quinolinic acid‐induced mitochondrial dysfunction in rat striatum
Author(s) -
LuisGarcía Erika Rubí,
LimónPacheco Jorge Humberto,
SerranoGarcía Norma,
HernándezPérez Alma Delia,
PedrazaChaverri José,
OrozcoIbarra Marisol
Publication year - 2017
Publication title -
journal of biochemical and molecular toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.526
H-Index - 58
eISSN - 1099-0461
pISSN - 1095-6670
DOI - 10.1002/jbt.21837
Subject(s) - quinolinic acid , sulforaphane , excitotoxicity , neuroprotection , mitochondrion , oxidative stress , striatum , chemistry , neuroscience , biology , microbiology and biotechnology , pharmacology , biochemistry , glutamate receptor , amino acid , tryptophan , receptor , dopamine
Quinolinic acid (QA) triggers striatal neuronal death by an excitotoxic cascade that involves oxidative stress, which in turns is tightly linked to mitochondria. Mitochondrial dysfunction is a molecular feature described in several brain pathologies. In this work, we determined whether the sulforaphane‐neuroprotective effect in the rodent experimental model of Huntington's disease induced by QA is associated with mitochondrial function preservation. We found that QA impaired mitochondrial function within 24 h post‐lesion. Sulforaphane effectively disrupted the mitochondrial dysfunction by preventing the decrease in respiratory control ratio, transmembrane potential, ability to synthetize ATP, and the activity of mitochondrial complexes I, II, and IV.