Decreased Glucose Utilization Contributes to Memory Impairment in Patients with Glufosinate Ammonium Intoxication

Abstract

The symptoms of glufosinate ammonium (GLA) intoxication include gastrointestinal and neurologic symptoms, respiratory failure, and cardiovascular instability. Among these, neurologic symptoms including loss of consciousness, memory impairment, and seizure are characteristic of GLA poisoning. However, the mechanism of brain injury by GLA poisoning is still poorly understood. We investigated nine patients who had performed an F-18 fluorodeoxyglucose (FDG) positron emission tomography (PET) scan because of memory impairment caused by GLA ingestion. FDG-PET images of patients with GLA intoxication were compared with 24 age- and sex-matched healthy controls to evaluate whether the patients had abnormal patterns of glucose metabolism in the brain. Decreased glucose metabolism was observed in the inferior frontal and temporal lobes of these patients with GLA intoxication when compared with 24 age- and sex-matched healthy controls. Three patients performed follow-up FDG-PET scans. However, it was shown that the results of the follow-up FDG-PET scans were determined to be inconclusive. Our study showed that memory impairment induced by GLA intoxication was associated with glucose hypometabolism in the inferior frontal and temporal lobes in the brain.

Prediction Model of Acute Respiratory Failure in Patients with Acute Pesticide Poisoning by Intentional Ingestion: Prediction of Respiratory Failure in Pesticide Intoxication (PREP) Scores in Cohort Study

“…The exact mechanism of respiratory failure in glufosinate poisoning has not been fully revealed. We previously reported that brain glucose metabolism decreased in patients with glufosinate intoxication [28]. Also, Park et al reported that the inhibition of both glycolysis and mitochondrial respiration pathway might be associated with oxidative stress and ferroptosis in human astrocytes [29].…”

“…Also, Park et al reported that the inhibition of both glycolysis and mitochondrial respiration pathway might be associated with oxidative stress and ferroptosis in human astrocytes [29]. Given the role of astrocytes in glucose metabolism and putative mechanisms associated with glufosinate [28], respiratory failure in glufosinate intoxication might be attributed to impairment of glucose metabolism. We hope further study could reveal the mechanism of respiratory failure in glufosinate poisoning.…”

Clinical features and prognostic factors of acute glufosinate ammonium

“…The median time for consciousness and convulsion or seizure was 33.0 (26.0, 40.0) hours and 45.0 (37.5, 48.5) hours after ingesting GA, respectively. Inhibition of glutamine synthetase by glufosinate ammonium may lead to elevated blood ammonia levels that are related to neurotoxicity symptoms [15]. Glutamine synthetase is a crucial enzyme in the human body that plays a critical role in brain metabolism and the normal function of various organs [16].…”

Prolonged cognitive dysfunction in patient with splenial lesion of the corpus callosum caused by glufosinate ammonium poisoning

“…They suggested that glucose hypometabolism could lead to long-lasting memory impairment regardless of structural brain lesions. [ 7 ]…”