Organophosphate (OP)-induced delayed neurotoxicity (OPIDN) is an axonopathy which is characterized by distal degeneration of some long and large-diameter axons in the peripheral nerves. In sensitive species, OPIDN is initiated when neuropathy target esterase (NTE) is inhibited and aged. A species specific susceptibility to OPIDN has been demonstrated.Adult hens have been widely used as the animal model for experimental studies of OPIDN due to their sensitivity and the development of clinical signs similar to those seen in humans. In contrast, mice, a widely used model animal, is insensitive to sign expression of OPIDN. Unfortunately, the mechanism responsible for neurotoxicity of OPs and different presentation of signsin mice and hens those are exposed to neuropathic OPs has not been elucidated.

Professor Yi-Jun Wu and his team (Laboratory of Molecular Toxicology in the Institute of Zoology, Chinese Academy of Sciences) investigated the alteration of NTE, lysophopholipase (LysoPLA) and phospholipase B (PLB) activities and the homeostasis of phosphatidylcholine (PC) and lysophosphatidylcholine (LPC)in nervous tissues of hens and mice treated with tri-ortho-cresyl phosphate (TOCP), the prototype delayed neurotoxicity-inducing agent. The results demonstrated that the PC and LPC homeostasis was not disrupted in nervous tissues of hens and mice after administration of TOCP. However, the inhibition of NTE, LysoPLA and PLB exhibited different characteristics between mice and hens. This indicated that difference in the inhibition of NTE, LysoPLA and PLB activities by TOCP between mice and hens may be the reason why these two species display different signs after exposure to the same neuropathic OPs.

The results of this work were recently published in Toxicological Sciences (Wei-Yuan Hou, Ding-Xin Long, Yi-Jun Wu. Toxicological Sciences 2009, 109:276-285.) and Toxicology (Hou W-Y, Long D-X, Wang H-P, Wang Q, Wu Y-J. Toxicology. 2008, 252:56-63.)