Hyperammonemia following glufosinate-containing herbicide poisoning: a potential marker of severe neurotoxicity

Clin Toxicol (Phila). 2011 Jan;49(1):48-52. doi: 10.3109/15563650.2010.539184.

Abstract

Glufosinate-ammonium (GLA) is the active ingredient of certain widely used non-selective contact herbicides ("e.g.," Basta). Although it is thought to be much less toxic to humans than to plants, deliberate ingestion of GLA could still lead to serious effects ("e.g.," neurotoxicity) or even death. Three cases presented with delayed-onset neurotoxicity including stupor, delirium, seizures, coma, and amnesia after ingesting large amount of Basta. Considering that GLA could irreversibly inhibit glutamine synthetase (GS) in plants, we performed serial measurements of serum ammonia in those patients and revealed marked hyperammonemia in all of them. All patients recovered with the sequelae of persistent amnesia after receiving intensive care and hemodialysis. We speculated that the occurrence of hyperammonemia might at least be partially related to GS inhibition in humans. Moreover, hyperammonemia could serve as a potential marker of severe neurotoxicity, especially prolonged amnesia, following massive ingestion of GLA-containing herbicides. The possible dose-response relation between GLA exposure and serum ammonia level, however, needs more investigations.

Publication types

  • Case Reports

MeSH terms

  • Adult
  • Aged
  • Aminobutyrates / poisoning*
  • Biomarkers
  • Female
  • Glutamate-Ammonia Ligase / antagonists & inhibitors
  • Herbicides / poisoning*
  • Humans
  • Hyperammonemia / chemically induced*
  • Male
  • Neurotoxicity Syndromes / diagnosis*

Substances

  • Aminobutyrates
  • Biomarkers
  • Herbicides
  • phosphinothricin
  • Glutamate-Ammonia Ligase