Advanced Glycation Endproducts Induce Changes in Glucose Consumption, Lactate Production, and ATP Levels in SH-SY5Y Neuroblastoma Cells by a Redox-Sensitive Mechanism

Susana Garcia De Arriba, Claudia Loske, Ina Meiners, Gerd Fleischer, Michael Lobisch, Klaus Wessel, Hans Tritschler, Reinhard Schinzel, Gerald Münch

Research output: Contribution to journalArticlepeer-review

26 Citations (Scopus)

Abstract

Advanced glycation endproducts (AGEs) accumulate on long-lived proteins, including β-amyloid plaques in Alzheimer's disease, and are suggested to contribute to neuronal dysfunction and cell death. We have investigated the effects of a model AGE upon glucose metabolism and energy production in a neuroblastoma cell line. AGEs decrease cellular ATP levels and increase glucose consumption and lactate production. All of the AGE-induced metabolic changes can be attenuated by antioxidants such as (R+)-α-lipoic acid and 17β-estradiol. These antioxidants may become useful drugs against (AGE-mediated) effects in neurodegeneration through their positive effects on cellular energy metabolism.

Original languageEnglish
Pages (from-to)1307-1313
Number of pages7
JournalJournal of Cerebral Blood Flow and Metabolism
Volume23
Issue number11
DOIs
Publication statusPublished - Nov 2003
Externally publishedYes

Keywords

  • Advanced glycation endproducts
  • Antioxidants
  • Lactate
  • Lipoic acid
  • Oxidative stress

Fingerprint

Dive into the research topics of 'Advanced Glycation Endproducts Induce Changes in Glucose Consumption, Lactate Production, and ATP Levels in SH-SY5Y Neuroblastoma Cells by a Redox-Sensitive Mechanism'. Together they form a unique fingerprint.

Cite this