The cytosolic redox state of astrocytes: Maintenance, regulation and functional implications for metabolite trafficking

被引:139
作者
Hirrlinger, Johannes [2 ]
Dringen, Ralf [1 ,3 ,4 ]
机构
[1] Univ Bremen, Fac Biol Chem 2, Ctr Biomol Interact Bremen, D-28334 Bremen, Germany
[2] Univ Leipzig, Interdisciplinary Ctr Clin Res, D-04103 Leipzig, Germany
[3] Ctr Environm Res & Sustainable Technol, D-28359 Bremen, Germany
[4] Monash Univ, Sch Psychol & Psychiat, Clayton, Vic 3800, Australia
关键词
Glutathione; Lactate; Metabolite trafficking; NADH; NADPH; Reduction potential; CULTURED ASTROGLIAL CELLS; CENTRAL-NERVOUS-SYSTEM; NICOTINAMIDE ADENINE-DINUCLEOTIDE; AWAKE CEREBRAL-CORTEX; HYDROGEN-PEROXIDE; GLYCERALDEHYDE-3-PHOSPHATE DEHYDROGENASE; GLUTATHIONE-REDUCTASE; SPREADING DEPRESSION; MOLECULAR-MECHANISMS; S-GLUTATHIONYLATION;
D O I
10.1016/j.brainresrev.2009.10.003
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Astrocytes have important functions in the metabolism of the brain. These cells provide neurons with metabolic substrates for energy production as well as with precursors for neurotransmitter and glutathione synthesis. Both the metabolism of astrocytes and the subsequent supply of metabolites from astrocytes to neurons are strongly affected by alterations in the cellular redox state. The cytosolic redox state of astrocytes depends predominantly on the ratios of the oxidised and reduced partners of the redox pairs NADH/NAD(+), NADPH/NADP(+) and GSH/GSSG. The NADH/NAD(+) pair is predominately in the oxidised state to accept electrons that are produced during glycolysis. In contrast, the redox pairs NADPH/NADP(+) and GSH/GSSG are biased towards the reduced state under unstressed conditions to provide electrons for reductive biosyntheses and antioxidative processes, respectively. In this review article we describe the metabolic processes that maintain the redox pairs in their desired redox states in the cytosol of astrocytes and discuss the consequences of alterations of the normal redox state for the regulation of cellular processes and for metabolite trafficking from astrocytes to neurons. (C) 2009 Elsevier B.V. All rights reserved.
引用
收藏
页码:177 / 188
页数:12
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