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Metabolic Brain Disease

, Volume 27, Issue 4, pp 531–539 | Cite as

Methylglyoxal alters glucose metabolism and increases AGEs content in C6 glioma cells

  • Fernanda Hansen
  • Daniela Fraga de Souza
  • Simone da Luz Silveira
  • Ana Lúcia Hoefel
  • Júlia Bijoldo Fontoura
  • Ana Carolina Tramontina
  • Larissa Daniele Bobermin
  • Marina Concli Leite
  • Marcos Luiz Santos Perry
  • Carlos Alberto GonçalvesEmail author
Original Paper

Abstract

Methylglyoxal is a dicarbonyl compound that is physiologically produced by enzymatic and non-enzymatic reactions. It can lead to cytotoxicity, which is mainly related to Advanced Glycation End Products (AGEs) formation. Methylglyoxal and AGEs are involved in the pathogenesis of Neurodegenerative Diseases (ND) and, in these situations, can cause the impairment of energetic metabolism. Astroglial cells play critical roles in brain metabolism and the appropriate functioning of astrocytes is essential for the survival and function of neurons. However, there are only a few studies evaluating the effect of methylglyoxal on astroglial cells. The aim of this study was to evaluate the effect of methylglyoxal exposure, over short (1 and 3 h) and long term (24 h) periods, on glucose, glycine and lactate metabolism in C6 glioma cells, as well as investigate the glyoxalase system and AGEs formation. Glucose uptake and glucose oxidation to CO2 increased in 1 h and the conversion of glucose to lipids increased at 3 h. In addition, glycine oxidation to CO2 and conversion of glycine to lipids increased at 1 h, whereas the incorporation of glycine in proteins decreased at 1 and 3 h. Methylglyoxal decreased glyoxalase I and II activities and increased AGEs content within 24 h. Lactate oxidation and lactate levels were not modified by methylglyoxal exposure. These data provide evidence that methylglyoxal may impair glucose metabolism and can affect glyoxalase activity. In periods of increased methylglyoxal exposure, such alterations could be exacerbated, leading to further increases in intracellular methylglyoxal and AGEs, and therefore triggering and/or worsening ND.

Keywords

AGEs Methylglyoxal C6 glioma cells Energetic metabolism Glyoxalase system 

Notes

Acknowledgements

We would like to thank Ms. Gisele Souza for technical support with cell culture. This work was supported by the Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq), Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES), FINEP/ Rede IBN 01.06.0842-00 and INCT-National Institute of Science and Technology for Excitotoxicity and Neuroprotection.

Conflict of interest

The authors declare that they have no conflict of interest.

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Copyright information

© Springer Science+Business Media, LLC 2012

Authors and Affiliations

  • Fernanda Hansen
    • 1
  • Daniela Fraga de Souza
    • 1
  • Simone da Luz Silveira
    • 1
  • Ana Lúcia Hoefel
    • 1
  • Júlia Bijoldo Fontoura
    • 2
  • Ana Carolina Tramontina
    • 1
  • Larissa Daniele Bobermin
    • 1
  • Marina Concli Leite
    • 1
  • Marcos Luiz Santos Perry
    • 1
  • Carlos Alberto Gonçalves
    • 1
    Email author
  1. 1.Departamento de Bioquímica, Instituto de Ciências Básicas da SaúdeUniversidade Federal do Rio Grande do SulPorto AlegreBrazil
  2. 2.Faculdade de FarmáciaUniversidade Federal do Rio Grande do SulPorto AlegreBrazil

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