Pathophysiological concentrations of ammonia, both in vivo and in vitro, suppressed the production of14CO2from14C-labelled glutamate and aspartate in astrocytes isolated from the rat cerebellum. Suppression of14CO2production with (aminooxy)acetic acid but not with glutamic acid diethyl ester indicated that transamination plays a major role in the oxidation of glutamate carbons. Activities of the enzymes, aspartate aminotransferase, alanine aminotransferase and glutaminase were decreased while those of glutamate dehydrogenase and glutamine synthetase were enhanced in the cerebellar astrocytes during hyperammonemic states. These results suggest an impairment of astrocytic glutamate metabolism during hyperammonemia. © 1992.
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