Hyperammonemia: regulation of argininosuccinate synthetase and argininosuccinate lyase genes in aggregating cell cultures of fetal rat brain.
- Braissant O Central Clinical Chemistry Laboratory, University Hospital, Lausanne, Switzerland. olivier.braissant@chuv.hospvd.ch
- Honegger P
- Loup M
- Iwase K
- Takiguchi M
- Bachmann C
- 1999-06-03
Published in:
- Neuroscience letters. - 1999
Ammonia
Animals
Argininosuccinate Lyase
Argininosuccinate Synthase
Brain
Cell Aggregation
Cells, Cultured
Embryonic and Fetal Development
Gene Expression Regulation, Developmental
Gene Expression Regulation, Enzymologic
Rats
English
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 AL 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.
- Language
-
- English
- Open access status
- green
- Identifiers
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- DOI 10.1016/s0304-3940(99)00274-8
- PMID 10353334
- Persistent URL
- https://sonar.ch/global/documents/189459
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