Advanced glycation endproducts induce changes in glucose consumption, lactate production, and ATP levels in SH-SY5Y neuroblastoma cells by a redox-sensitive mechanism.
Advanced glycation endproducts (AGEs) accumulate on long-lived proteins, including beta-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+)-alpha-lipoic acid and 17beta-estradiol. These antioxidants may become useful drugs against (AGE-mediated) effects in neurodegeneration through their positive effects on cellular energy metabolism.
Neuroimmunological Cell Biology Unit, Leipzig, Germany.
Susana Garcia
SG
de Arriba
Claudia
C
Loske
Ina
I
Meiners
Gerd
G
Fleischer
Michael
M
Lobisch
Klaus
K
Wessel
Hans
H
Tritschler
Reinhard
R
Schinzel
Gerald
G
Münch
D000255:Adenosine Triphosphate / Q000378:metabolism*; D000975:Antioxidants / Q000494:pharmacology; D045744:Cell Line, Tumor; D004305:Dose-Response Relationship, Drug; D004734:Energy Metabolism; D004958:Estradiol / Q000494:pharmacology; D005947:Glucose / Q000378:metabolism*; D017127:Glycation End Products, Advanced / Q000494:pharmacology*; D006801:Humans; D007700:Kinetics; D007773:Lactates / Q000378:metabolism*; D009447:Neuroblastoma / Q000473:pathology*; D010084:Oxidation-Reduction; D008063:Thioctic Acid / Q000494:pharmacology
D000975:Antioxidants; D017127:Glycation End Products, Advanced; D007773:Lactates; D004958:Estradiol; D008063:Thioctic Acid; D000255:Adenosine Triphosphate; D005947:Glucose