Homocysteine increases neuronal damage in hippocampal slices receiving oxygen and glucose deprivation

被引：24

作者：

Tagliari, Barbara ^{[1
]}

Zamin, Lauren L. ^{[1
]}

Salbego, Christianne G. ^{[1
]}

Netto, Carlos Alexandre ^{[1
]}

Wyse, Angela T. S. ^{[1
]}

机构：

[1] Univ Fed Rio Grande do Sul, ICBS, Dept Bioquim, BR-90035003 Porto Alegre, RS, Brazil

来源：

METABOLIC BRAIN DISEASE | 2006年 / 21卷 / 04期

关键词：

homocysteine; homocystinuria; metabolic disease; cerebral ischemia; cell damage;

D O I：

10.1007/s11011-006-9029-y

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Homocystinuria is an inherited metabolic disorder caused by severe deficiency of cystationine beta-synthase activity, resulting in the tissue accumulation of homocysteine (Hcy). Affected patients usually present many signs and symptoms such as seizures, mental retardation, atherosclerosis and stroke. The aim of this study is to evaluate in vivo and in vitro effects of Hcy using hippocampal slices from Wistar rats exposed to oxygen and glucose deprivation (OGD), followed by reoxygenation, an in vitro model of hypoxic-ischemic events. Neural cell injury was quantified by the measurement of lactate dehydrogenase (LDH) released from damaged cells into the extracellular fluid. The results showed that both in vivo and in vitro Hcy increased the LDH released to de incubation medium, suggesting an increase of tissue damage caused by OGD. This fact can be related with the high incidence of stroke in homocystinuric patients.

引用

页码：273 / 278

页数：6

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