Chemical Modification of Taipoxin and the Consequences for Phospholipase Activity, Pathophysiology, and Inhibition of High-Affinity Choline Uptake



Treatment of taipoxin with p-bromophenacyl bromide resulted in modification of single histidine residues in the α and β subunits. The modification decreased the neurotoxicity (lethality) 350-fold, but the inhibitory action on high-affinity choline transport was reduced only threefold. The phospholipase activity and Ca2+-association constants for taipoxin and its subunits were determined. A model for the neurotoxicity of taipoxin indicates the α subunit as the ultimate cause of the disruption of synaptic transmission.