Related Experiment Videos
Hyperammonemia causes altered protein phosphorylation in astrocytes
J T Neary1, L O Norenberg, M P Gutierrez
1Laboratory of Neuropathology, Veterans Administration Medical Center, Miami, FL.
Brain Research
|December 22, 1987
Summary
Ammonia exposure reduces phosphate incorporation in a specific 66-kDa protein in astrocytes. This suggests altered protein phosphorylation may contribute to ammonia-related brain disorders like hepatic encephalopathy.
Area of Science:
- Neuroscience
- Biochemistry
- Cell Biology
Background:
- Ammonia is implicated in the pathogenesis of hepatic encephalopathy and Reye's syndrome.
- Altered protein phosphorylation is a potential mechanism in neurological disorders.
Purpose of the Study:
- To investigate the effect of ammonia on protein phosphorylation in primary astrocyte cultures.
- To determine if ammonia exposure alters the phosphorylation of specific proteins.
Main Methods:
- Primary astrocyte cultures were treated with varying concentrations of ammonium chloride (2, 5, 10 mM).
- Phosphoprotein labeling was performed to assess phosphate incorporation.
- Protein phosphorylation levels were analyzed using gel electrophoresis.
Main Results:
- Ammonium chloride treatment reduced phosphate incorporation in a 66-kDa protein.
- The reduction in phosphate incorporation was dose-dependent with increasing ammonium chloride concentrations.
- Phosphate incorporation in seven other protein bands remained unchanged, indicating specificity.
Conclusions:
- Pathophysiological concentrations of ammonia can affect protein phosphorylation in astrocytes.
- Altered protein phosphorylation may play a role in the pathogenesis of ammonia-related neurological disorders.
- This finding provides a potential molecular mechanism for conditions like hepatic encephalopathy and Reye's syndrome.