Effects of variations in glutamic acid decarboxylase activity on acute oxygen poisoning.
A study was made to test the influence of rapid variations in glutamic acid decarboxylase (GAD) activity on the susceptibility of rats to hyperbaric oxygen (HBO). GAD was inhibited by the convulsant drug unsymmetrical dimethylhydrazine (UDMH) and reactivated by pyridoxine (PYR) after onset of convulsive activity. There was a relatively long induction period after UDMH injection until the onset of convulsions and the predictable interictal periods between successive periodic convulsions made it possible to study the impact of variations in GAD activity on survival rates, suspectibility to HBO and brain glycogen levels in a time sequence after UDMH administration. The experiments showed that UDMH interferes with aerobic metabolism in brain in such a way that profound alterations in resistance to acute oxygen poisoning resulted. An accumulation of substrate proximal to the enzyme block is assumed to develop during UDMH poisoning. The protective effect against HBO toxicity that was achieved after reactivation of GAD by PYR injection, as well as the rapid re-establishment of glycogen levels, is believed to speak in favour of this hypothesis.
D000818:Animals; D001921:Brain / Q000378:metabolism*; D002262:Carboxy-Lyases / Q000378:metabolism*; D005968:Glutamate Decarboxylase / Q000378:metabolism*; D006003:Glycogen / Q000378:metabolism; D006931:Hyperbaric Oxygenation; D007700:Kinetics; D008297:Male; D010100:Oxygen / Q000506:poisoning*; D011736:Pyridoxine / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D012640:Seizures / Q000378:metabolism
D006003:Glycogen; D002262:Carboxy-Lyases; D005968:Glutamate Decarboxylase; D011736:Pyridoxine; D010100:Oxygen