Changes in the activity of gamma-glutamyl transpeptidase in brain microvessels, astroglial cells and synaptosomes derived from rats with hepatic encephalopathy
Language English Country Ireland Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
2895441
DOI
10.1016/0304-3940(88)90529-0
PII: 0304-3940(88)90529-0
Knihovny.cz E-resources
- MeSH
- Astrocytes enzymology MeSH
- gamma-Glutamyltransferase metabolism MeSH
- Rats, Inbred Strains MeSH
- Liver drug effects enzymology pathology MeSH
- Capillaries enzymology MeSH
- Rats MeSH
- Brain enzymology MeSH
- Cerebrovascular Circulation * MeSH
- Liver Diseases enzymology MeSH
- Synaptosomes enzymology MeSH
- Thioacetamide toxicity MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- gamma-Glutamyltransferase MeSH
- Thioacetamide MeSH
Prolonged thioacetamide treatment increased gamma-glutamyl transpeptidase (GGT) activity in the rat liver and induced neurological symptoms of hepatic encephalopathy (HE). The enzyme activity measured without an amino acid or peptide acceptor was increased in cortical capillaries and synaptosomes, but remained unchanged in astroglia isolated from the brains of hyperammonemic rats. In the presence of L-glutamine the activity of GGT was stimulated by about 60% in astroglial cells while in the capillaries and synaptosomes the amino acid stimulation was less pronounced. Glycylglycine also stimulated the GGT activity in the astroglia more (4-fold) than in cortical capillaries or synaptosomes (3-fold). Similar stimulatory effects of these gamma-glutamyl moiety acceptors on the GGT activity were observed in capillaries, glial cells and synaptosomes derived from the brains of rats with HE. These results indicate that GGT may be involved in the excessive accumulation of large neutral amino acids (and some peptides) in the brain of rats with HE.
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