Neonatal hyperglycemia induces oxidative stress in the rat brain: the role of pentose phosphate pathway enzymes and NADPH oxidase
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  • 作者:Andrea Pereira Rosa (2)
    Carlos Eduardo Dias Jacques (1)
    Laila Oliveira de Souza (1)
    Fernanda Bitencourt (1)
    Priscila Nicolao Mazzola (2)
    Juliana Gonzales Coelho (2)
    Caroline Paula Mescka (2)
    Carlos Severo Dutra-Filho (1) (2)

    2. Programa de P贸s-Gradua莽茫o em Ci锚ncias Biol贸gicas
    ; Bioqu铆mica ; Instituto de Ci锚ncias B谩sicas da Sa煤de ; Universidade Federal do Rio Grande do Sul ; Porto Alegre ; RS ; Brazil
    1. Departamento de Bioqu铆mica
    ; Instituto de Ci锚ncias B谩sicas da Sa煤de ; Universidade Federal do Rio Grande do Sul ; Rua Ramiro Barcelos ; 2600 (Anexo) ; Porto Alegre ; RS ; 90035-003 ; Brazil
  • 关键词:Neonatal hyperglycemia ; NADPH oxidase ; Glucose ; 6 ; phosphate ; dehydrogenase ; Superoxide ; Oxidative stress ; Brain
  • 刊名:Molecular and Cellular Biochemistry
  • 出版年:2015
  • 出版时间:May 2015
  • 年:2015
  • 卷:403
  • 期:1-2
  • 页码:159-167
  • 全文大小:340 KB
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  • 刊物类别:Biomedical and Life Sciences
  • 刊物主题:Life Sciences
    Biochemistry
    Medical Biochemistry
    Oncology
    Cardiology
  • 出版者:Springer Netherlands
  • ISSN:1573-4919
文摘
Recently, the consequences of diabetes on the central nervous system (CNS) have received great attention. However, the mechanisms by which hyperglycemia affects the central nervous system remain poorly understood. In addition, recent studies have shown that hyperglycemia induces oxidative damage in the adult rat brain. In this regard, no study has assessed oxidative stress as a possible mechanism that affects the brain normal function in neonatal hyperglycemic rats. Thus, the present study aimed to investigate whether neonatal hyperglycemia elicits oxidative stress in the brain of neonate rats subjected to a streptozotocin-induced neonatal hyperglycemia model (5-day-old rats). The activities of glucose-6-phosphate-dehydrogenase (G6PD), 6-phosphogluconate-dehydrogenase (6-PGD), NADPH oxidase (Nox), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSHPx), the production of superoxide anion, the thiobarbituric acid-reactive substances (TBA-RS), and the protein carbonyl content were measured. Neonatal hyperglycemic rats presented increased activities of G6PD, 6PGD, and Nox, which altogether may be responsible for the enhanced production of superoxide radical anion that was observed. The enhanced antioxidant enzyme activities (SOD, CAT, and GSHPx) that were observed in neonatal hyperglycemic rats, which may be caused by a rebound effect of oxidative stress, were not able to hinder the observed lipid peroxidation (TBA-RS) and protein damage in the brain. Consequently, these results suggest that oxidative stress could represent a mechanism that explains the harmful effects of neonatal hyperglycemia on the CNS.

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