Critical Evaluation of the Changes in Glutamine Synthetase Activity in Models of Cerebral Stroke

被引:32
|
作者
Jeitner, Thomas M. [1 ]
Battaile, Kevin [2 ]
Cooper, Arthur J. L. [1 ]
机构
[1] New York Med Coll, Dept Biochem & Mol Biol, Valhalla, NY 10595 USA
[2] Argonne Natl Lab, 9700 S Cass Ave, Argonne, IL 60439 USA
关键词
Brain; Glutamine synthetase; Ischemia-reperfusion; Oxidative stress; Stroke; PROTEIN-TYROSINE NITRATION; RECEPTOR-MEDIATED RESPONSES; MILD COGNITIVE IMPAIRMENT; MIXED-FUNCTION OXIDATION; D-ASPARTIC ACID; NITRIC-OXIDE; RAT-BRAIN; IN-VIVO; ALZHEIMERS-DISEASE; MOUSE MODEL;
D O I
10.1007/s11064-015-1667-1
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 following article addresses some seemingly paradoxical observations concerning cerebral glutamine synthetase in ischemia-reperfusion injury. In the brain, this enzyme is predominantly found in astrocytes and catalyzes part of the glutamine-glutamate cycle. Glutamine synthetase is also thought to be especially sensitive to inactivation by the oxygen-and nitrogen-centered radicals generated during strokes. Despite this apparent sensitivity, glutamine synthetase specific activity is elevated in the affected tissues during reperfusion. Given the central role of the glutamine-glutamate cycle in the brain, we sought to resolve these conflicting observations with the view of providing an alternative perspective for therapeutic intervention in stroke.
引用
收藏
页码:2544 / 2556
页数:13
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