Premium
Effect of glycolysis inhibition on mitochondrial function in rat brain
Author(s) -
CanoRamírez D.,
TorresVargas C. E.,
GuerreroCastillo S.,
UribeCarvajal S.,
HernándezPando R.,
PedrazaChaverri J.,
OrozcoIbarra M.
Publication year - 2012
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.21404
Subject(s) - aconitase , glycolysis , oxidative stress , mitochondrion , excitotoxicity , glyceraldehyde 3 phosphate dehydrogenase , biochemistry , reactive oxygen species , citric acid cycle , glutathione , chemistry , oxidative phosphorylation , biology , endocrinology , medicine , dehydrogenase , enzyme , programmed cell death , apoptosis
Inhibition of the glycolytic enzyme glyceraldehyde‐3‐phosphate dehydrogenase enhances the neural vulnerability to excitotoxicity both in vivo and in vitro through an unknown mechanism possibly related to mitochondrial failure. However, as the effect of glycolysis inhibition on mitochondrial function in brain has not been studied, the aim of the present work was to evaluate the effect of glycolysis inhibition induced by iodoacetate on mitochondrial function and oxidative stress in brain. Mitochondria were isolated from brain cortex, striatum and cerebellum of rats treated systemically with iodoacetate (25 mg/kg/day for 3 days). Oxygen consumption, ATP synthesis, transmembrane potential, reactive oxygen species production, lipoperoxidation, glutathione levels, and aconitase activity were assessed. Oxygen consumption and aconitase activity decreased in the brain cortex and striatum, showing that glycolysis inhibition did not trigger severe mitochondrial impairment, but a slight mitochondrial malfunction and oxidative stress were present. © 2012 Wiley Periodicals, Inc. J Biochem Mol Toxicol 26:206–211, 2012; View this article online at wileyonlinelibrary.com . DOI 10.1002/jbt.21404