Hyperammonemia: regulation of argininosuccinate synthetase and argininosuccinate lyase genes in aggregating cell cultures of fetal rat brain

被引：43

作者：

Braissant, O ^{[1
]}

Honegger, P

Loup, M

Iwase, K

Takiguchi, M

Bachmann, C

机构：

[1] Univ Lausanne Hosp, Cent Lab Clin Chem, CH-1011 Lausanne, Switzerland

[2] Univ Lausanne, Inst Physiol, CH-1011 Lausanne, Switzerland

[3] Kumamoto Univ, Sch Med, Dept Mol Genet, Kumamoto 8620976, Japan

来源：

NEUROSCIENCE LETTERS | 1999年 / 266卷 / 02期

关键词：

brain; argininosuccinate; arginine; citrulline-NO cycle; astrocyte; hyperammonemia;

D O I：

10.1016/S0304-3940(99)00274-8

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Hyperammonemia in the brain leads to poorly understood alterations of nitric oxide (NO) synthesis. Arginine, the substrate of nitric oxide synthases, might be recycled from the citrulline produced with NO by argininosuccinate synthetase (AS) and argininosuccinate lyase (AL). The regulation of AS and At genes during hyperammonemia is unknown in the brain. We used brain cell aggregates cultured from dissociated telencephalic cortex of rat embryos to analyze the regulation of AS and AL genes in hyperammonemia. Using RNase protection assay and non-radioactive in situ hybridization on aggregate cryosections, we show that both AS and AL genes are induced in astrocytes but not in neurons of aggregates exposed to 5 mM NH4Cl. Our work suggests that the hyperammonemic brain might increase its recycling of citrulline to arginine. (C) 1999 Elsevier Science ireland Ltd. All rights reserved.

引用

页码：89 / 92

页数：4

共 17 条

[1] AMINO-ACID SEQUENCE OF RAT ARGININOSUCCINATE LYASE DEDUCED FROM CDNA [J].