Abstract

The effect of oxygen at high pressure (OHP) on the γ-aminobutyric acid (GABA) shunt pathway in rat brain homogenates was studied by measuring the formation of labelled succinate from GABA-4-14C in the presence of malonate. Under in vitro conditions, OHP inhibited the GABA shunt by 28% and 22%, with and without the addition of supplementary amounts of GABA and α-ketoglutarate to the incubation media respectively. A small inhibition (10%) was also observed with oxygen at ambient pressure. In further studies, rats were exposed to OHP, and the activity of the GABA shunt in the brains was subsequently measured by the in vitro method. Preexposure of the intact animals, with or without accompanying convulsions, did not affect the metabolism of GABA to succinate.

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