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Oxidative Medicine and Cellular Longevity
Volume 2013, Article ID 607610, 8 pages
http://dx.doi.org/10.1155/2013/607610
Research Article

Neurotoxic Effects of trans-Glutaconic Acid in Rats

1Laboratório de Erros Inatos do Metabolismo, Programa de Pós-graduação em Ciências da Saúde, Unidade Acadêmica de Ciências da Saúde, Universidade do Extremo Sul Catarinense, 88806-000 Criciúma, SC, Brazil
2Núcleo de Excelência em Neurociências Aplicadas de Santa Catarina (NENASC), Programa de Pós-Graduação em Ciências da Saúde, Unidade Acadêmica de Ciências da Saúde, Universidade do Extremo Sul Catarinense, 88806-000 Criciúma, SC, Brazil
3Departamento de Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, 90035-003 Porto Alegre, RS, Brazil

Received 9 January 2013; Revised 3 March 2013; Accepted 4 March 2013

Academic Editor: Emilio Luiz Streck

Copyright © 2013 Patrícia F. Schuck et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

trans-Glutaconic acid (tGA) is an unsaturated C5-dicarboxylic acid which may be found accumulated in glutaric aciduria type I, whose pathophysiology is still uncertain. In the present work it was investigated the in vitro effect of increasing tGA concentrations on neurochemical and oxidative stress parameters in rat cerebral cortex. We observed that Na+, K+-ATPase activity was reduced by tGA, but not creatine kinase, respiratory chain complex IV, and ATP synthase activities. On the other hand, tGA significantly increased lipid peroxidation (thiobarbituric acid-reactive species levels and spontaneous chemiluminescence), as well as protein oxidative damage (oxidation of sulfhydryl groups). tGA also significantly decreased nonenzymatic antioxidant defenses (TRAP and reduced glutathione levels). Our data suggest that tGA may be neurotoxic in rat brain.