Advanced glycation endproducts induce changes in glucose consumption, lactate production, and ATP levels in SH-SY5Y neuroblastoma cells by a redox-sensitive mechanism

被引：25

作者：

de Arriba, SG

Loske, C

Meiners, I

Fleischer, G

Lobisch, T

Wessel, K

Tritschler, H

Schinzel, T

Münch, G

机构：

[1] Interdisciplinary Ctr Clin Res IZKF, Neuroimmunol Cell Biol Unit, D-04103 Leipzig, Germany

[2] Univ Wurzburg, Bioctr, Wurzburg, Germany

[3] Viatris Pharma GmbH, Frankfurt, Germany

来源：

JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM | 2003年 / 23卷 / 11期

关键词：

advanced glycation endproducts; lactate; oxidative stress; lipoic acid; antioxidants;

D O I：

10.1097/01.WCB.0000090622.86921.0E

中图分类号：

R5 [内科学];

学科分类号：

1002 [临床医学]; 100201 [内科学];

摘要：

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.

引用

页码：1307 / 1313

页数：7

共 38 条

[1]

Controlled trial of N-acetyleysteine for patients with probable Alzheimer's disease [J].