Reactivation studies on organophosphate inhibited human cholinesterases by pralidoxime (P-2-AM).
There is biochemical and clinical evidence that P-2-AM (Pyridine-2-Aldoxime Methiodide, Pralidoxime) does not reactive human acetylcholinesterase inhibited by either Malathion or Malaoxon. In vitro studies using Pralidoxime iodide up to ten times the recommended concentrations, produced insignificant reactivation of cholinesterases inhibited by Malathion or Malaoxon. This was observed inspite of prolonged exposure of the inhibited cholinesterases to the oxime. The value of Pralidoxime as a reactivator of phosphorylated cholinesterases is therefore in doubt, and should not be used in preference to large doses of atropine and other supportive treatment in poisoning by organophosphate pesticides.
D000110:Acetylcholinesterase / Q000097:blood; D002091:Butyrylcholinesterase / Q000097:blood; D002800:Cholinesterase Inhibitors; D002802:Cholinesterases / Q000097:blood*; D004789:Enzyme Activation / Q000187:drug effects; D006801:Humans; D008294:Malathion / Q000031:analogs & derivatives* / Q000494:pharmacology*; D011220:Pralidoxime Compounds / Q000494:pharmacology*
D002800:Cholinesterase Inhibitors; D011220:Pralidoxime Compounds; D000110:Acetylcholinesterase; D002091:Butyrylcholinesterase; D002802:Cholinesterases; D008294:Malathion