Effect of glycolysis inhibition on mitochondrial function in rat brain

被引：16

作者：

Cano-Ramirez, D. ^{[2
]}

Torres-Vargas, C. E. ^{[2
]}

Guerrero-Castillo, S. ^{[3
]}

Uribe-Carvajal, S. ^{[3
]}

Hernandez-Pando, R. ^{[4
]}

Pedraza-Chaverri, J. ^{[2
]}

Orozco-Ibarra, M. ^{[1
]}

机构：

[1] Inst Nacl Neurol & Neurocirugia Manuel Velasco Su, Lab Neurobiol Mol & Celular, Mexico City 14269, DF, Mexico

[2] Univ Nacl Autonoma Mexico, Fac Quim, Dept Biol, Mexico City 04510, DF, Mexico

[3] Univ Nacl Autonoma Mexico, Inst Fisiol Celular, Dept Mol Genet, Mexico City 04510, DF, Mexico

[4] Inst Nacl Ciencias Med & Nutr Salvador Zubiran, Lab Patol Expt, Mexico City 14000, DF, Mexico

来源：

JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY | 2012年 / 26卷 / 05期

关键词：

Glycolysis Inhibition; Mitochondria; Brain; Iodoacetate; Oxidative Stress; MEDIATED NEURONAL DAMAGE; IN-VIVO; 3-NITROPROPIONIC ACID; HIPPOCAMPAL-NEURONS; OXIDATIVE STRESS; IODOACETATE; NEURODEGENERATION; NEUROTOXICITY; METABOLISM; ACTIVATION;

D O I：

10.1002/jbt.21404

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

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. (c) 2012 Wiley Periodicals, Inc. J Biochem Mol Toxicol 26:206211, 2012; View this article online at . DOI 10.1002/jbt.21404

引用

页码：206 / 211

页数：6

共 25 条

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