MECHANISM OF ACTION OF β‐N‐OXALYL‐L‐α, β‐DIAMINOPROPIONIC ACID, THE LATHYRUS SATIVUS NEUROTOXIN

Abstract

Abstract The source of ammonia in the brain tissue of young rats treated with β‐ N ‐oxalyl‐ l ‐α, β‐diaminopropionic acid (ODAP) has been studied. ODAP administration to 12‐day‐old rats causes a significant increase in the levels of adenylic acid deaminase in the brain. Glutaminase activity also shows an increase under these conditions. An increase in the levels of acid protease and transglutaminase is also observed in the brain of ODAP‐treated animals. Glutamate dehydrogenase activity is decreased slightly. Glutamine synthetase enzyme is not affected. Aspartate‐α‐ketoglutarate transaminase and aspartate‐pyruvate transaminase activities are enhanced in the brain tissue of ODAP‐treated rats. It is held that protein degradation, especially the cleavage of free and protein‐bound amide bonds, may be responsible for excess ammonia liberation in the brain of ODAP‐treated young rats.