Neuronal Death and Oxidative Stress in the Developing Brain

被引:203
作者
Ikonomidou, Chrysanthy [1 ,2 ]
Kaindl, Angela M. [3 ,4 ]
机构
[1] Univ Wisconsin, Dept Neurol, Madison, WI 53792 USA
[2] Univ Wisconsin, Waisman Ctr, Dev Brain Injury Lab, Madison, WI 53792 USA
[3] Charite, Ctr Anat, Dept Pediat Neurol, D-13353 Berlin, Germany
[4] Charite, Ctr Anat, Waisman Inst Cell Biol & Neurobiol, D-13353 Berlin, Germany
关键词
COPPER/ZINC-SUPEROXIDE-DISMUTASE; INDUCED CELL-DEATH; INDUCED APOPTOTIC NEURODEGENERATION; EXACERBATES CEREBRAL INFARCTION; REGIONAL ENZYME DEVELOPMENT; EARLY POSTNATAL ONTOGENY; EXCITATORY AMINO-ACIDS; HUMAN MOTOR CORTEX; ISCHEMIC BRAIN; RAT-BRAIN;
D O I
10.1089/ars.2010.3581
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The developing brain is particularly vulnerable to reactive oxygen and reactive nitrogen species-mediated damage because of its high concentrations of unsaturated fatty acids, high rate of oxygen consumption, low concentrations of antioxidants, high content of metals catalyzing free radical formation, and large proportion of sensitive immature cells. In this review, we outline the dynamic changes of energy resources, metabolic requirements, and endogenous free radical scavenging systems during physiologic brain development. We further discuss the involvement of oxidative stress in the pathogenesis of neuronal death after exposure of the infant brain to hyperoxia, hypoxia/ischemia, sedative drugs, ethanol, and mechanical trauma. Several approaches have been developed to combat oxidative stress, but neuroprotective treatment strategies are limited in the clinical setting. Antioxid. Redox Signal. 14, 1535-1550.
引用
收藏
页码:1535 / 1550
页数:16
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