THE OSMOTIC CALCIUM STRESS THEORY OF BRAIN-DAMAGE - ARE FREE-RADICALS INVOLVED

被引:51
作者
PAZDERNIK, TL
LAYTON, M
NELSON, SR
SAMSON, FE
机构
[1] UNIV KANSAS, MED CTR, RALPH L SMITH RES CTR, KANSAS CITY, KS 66103 USA
[2] UNIV KANSAS, DEPT ANAT & CELL BIOL, LAWRENCE, KS 66045 USA
关键词
LOCAL CEREBRAL GLUCOSE USE; EXCITATORY AMINO ACIDS; BRAIN OSMOREGULATION; BRAIN DAMAGE; REACTIVE OXYGEN SPECIES;
D O I
10.1007/BF00966860
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
This overview presents data showing that glucose use increases and that excitatory amino acids (i.e., glutamate, aspartate), taurine and ascorbate increase in the extracellular fluid during seizures. During the cellular hyperactive state taurine appears to serve as an osmoregulator and ascorbate may serve as either an antioxidant or as a pro-oxidant. Finally, a unifying hypothesis is given for seizure-induced brain damage. This unifying hypothesis states that during seizures there is a release of excitatory amino acids which act on glutamatergic receptors, increasing neuronal activity and thereby increasing glucose use. This hyperactivity of cells causes an influx of calcium (i.e., calcium stress) and water movements (i.e., osmotic stress) into the cells that culminate in brain damage mediated by reactive oxygen species.
引用
收藏
页码:11 / 21
页数:11
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