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Arginine in thioacetamide‐induced hepatogenic encephalopathy in rats: activation of enzymes of arginine metabolism to glutamate
Author(s) -
Albrecht J.,
Hilgier W.
Publication year - 1986
Publication title -
acta neurologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.967
H-Index - 95
eISSN - 1600-0404
pISSN - 0001-6314
DOI - 10.1111/j.1600-0404.1986.tb04593.x
Subject(s) - arginase , arginine , thioacetamide , ornithine , urea cycle , glutamate receptor , medicine , argininosuccinate synthase , endocrinology , chemistry , amino acid , enzyme , biochemistry , ornithine aminotransferase , hyperammonemia , metabolism , glutamine , biology , receptor
Two subsequent phases of hepatogenic encephalopathy (HE), the metabolic and precomatous phase, were produced in rats by thioacetamide treatment. Plasma and brain levels of arginine and its metabolites in the arginineglutamate pathway, and activities of 2 brain enzymes of this pathway: arginase (L‐arginine amidohydrolase, EC3521) and ornithine amino‐transferase (OAT, ornithineoxo‐acid aminotransferase, EC26113) were measured in these rats. Plasma arginine sharply decreased in the metabolic phase and rose above control level in the precomatous phase, whereas ornithine and glutamate increased and urea decreased in both phases. Brain amino acids levels remained unchanged throughout, confirming earlier report of their intensivity to external manipulation. Both brain enzymes showed a similar stepwise increase in their activities up to 150% the control level. The results are indicative of increased involvement of arginine as a precursor of amino acid neurotransmitters glutamate and GABA, with possible implication for the course of HE.