1. Effect of glycolysis inhibition on mitochondrial function in rat brain.
- Author
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Cano-Ramírez D, Torres-Vargas CE, Guerrero-Castillo S, Uribe-Carvajal S, Hernández-Pando R, Pedraza-Chaverri J, and Orozco-Ibarra M
- Subjects
- Adenosine Triphosphate biosynthesis, Animals, Glyceraldehyde-3-Phosphate Dehydrogenases antagonists & inhibitors, Iodoacetates pharmacology, Lipid Peroxidation drug effects, Membrane Potential, Mitochondrial drug effects, Oxygen Consumption drug effects, Rats, Reactive Oxygen Species metabolism, Brain drug effects, Brain enzymology, Glyceraldehyde-3-Phosphate Dehydrogenases metabolism, Glycolysis drug effects, Mitochondria drug effects, Mitochondria enzymology
- Abstract
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., (Copyright © 2012 Wiley Periodicals, Inc.)
- Published
- 2012
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