Carbonyl stress and NMDA receptor activation contribute to methylglyoxal neurotoxicity.

@article{Arriba2006CarbonylSA,
  title={Carbonyl stress and NMDA receptor activation contribute to methylglyoxal neurotoxicity.},
  author={Susana Garcia de Arriba and Ute Kr{\"u}gel and Ralf Regenthal and Zacharie Vissiennon and Esther Verdaguer and Anne Lewerenz and Elvira Garc{\'i}a-Jord{\'a} and Merc{\`e} Pall{\`a}s and Antoni Camins and Gerald M{\"u}nch and Karen Nieber and Clemens Allgaier},
  journal={Free radical biology & medicine},
  year={2006},
  volume={40 5},
  pages={779-90}
}
Methylglyoxal (MG) is a reactive alpha-ketoaldehyde physiologically generated as a by-product of glycolysis. MG that is able to form protein adducts resulting in advanced glycation end products accumulates under conditions associated with neurodegeneration such as impaired glucose metabolism or oxidative stress. In the present study, short-term exposure of human neuroblastoma SH-SY5Y cells to MG was associated with an early depolarization of the plasma membrane, glutamate release, and formation… CONTINUE READING

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