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Activation of arginine metabolism to glutamate in rat brain synaptosomes in thioacetamide‐induced hepatic encephalopathy: An adaptative response?
Author(s) -
Albrecht J.,
Hilgier W.,
Rafalowska U.
Publication year - 1990
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.490250116
Subject(s) - thioacetamide , arginine , glutamate receptor , neurotransmitter , arginase , chemistry , hepatic encephalopathy , catabolism , gamma aminobutyric acid , biochemistry , medicine , metabolism , synaptosome , endocrinology , amino acid , biology , cirrhosis , receptor , membrane
Crude (P2) synaptosomes derived from rats with acute hepatic encephalopathy (HE) induced with thioacetamide showed a slightly increased uptake of radiolabeled arginine (ARG) and a 2.5‐fold enhanced conversion of newly taken‐up ARG to both glutamate (GLU) and γ‐aminobutyric acid (GABA) as compared with control synaptosomes with a high potassium medium decreased their radioactive GLU and GABA content without affecting the content of the precursor ARG. This result, which was identical with control or HE preparations, appears to indicate that ARG contributes at least, in part, to the synthesis of neurotransmitter GLU or GABA. As measured in purified synaptosomal preparations, HE increased by about 50% the activities of arginase and ornithine‐δ‐aminotransferase‐the two enzymes of the ARG to GLU shunt. It is postulated that increased conversion of ARG to GLU may compensate for excessive utilization of the latter amino acid as an ammonia trap during HE and, as such, may be considered as an adaptative response of the synaptic compartment to this pathological condition.