| First Author | Duysen EG | Year | 2011 |
| Journal | Toxicol Appl Pharmacol | Volume | 255 |
| Issue | 2 | Pages | 214-20 |
| PubMed ID | 21767560 | Mgi Jnum | J:174614 |
| Mgi Id | MGI:5140245 | Doi | 10.1016/j.taap.2011.06.021 |
| Citation | Duysen EG, et al. (2011) Induction of plasma acetylcholinesterase activity in mice challenged with organophosphorus poisons. Toxicol Appl Pharmacol 255(2):214-20 |
| abstractText | The restoration of plasma acetylcholinesterase activity in mice following inhibition by organophosphorus pesticides and nerve agents has been attributed to synthesis of new enzyme. It is generally assumed that activity levels return to normal, are stable and do not exceed the normal level. We have observed over the past 10years that recovery of acetylcholinesterase activity levels in mice treated with organophosphorus agents (OP) exceeds pretreatment levels and remains elevated for up to 2months. The most dramatic case was in mice treated with tri-cresyl phosphate and tri-ortho-cresyl phosphate, where plasma acetylcholinesterase activity rebounded to a level 250% higher than the pretreatment activity. The present report summarizes our observations on plasma acetylcholinesterase activity in mice treated with chlorpyrifos, chlorpyrifos oxon, diazinon, tri-ortho-cresyl phosphate, tri-cresyl phosphate, tabun thiocholine, parathion, dichlorvos, and diisopropylfluorophosphate. We have developed a hypothesis to explain the excess acetylcholinesterase activity, based on published observations. We hypothesize that acetylcholinesterase activity is induced when cells undergo apoptosis and that consequently there is a rise in the level of plasma acetylcholinesterase. |
