Abstract: Organophosphates (OPs) are known to produce a delayed neuropathy in man and domestic animals. Other than acute cholinergic toxicity of OPs, they have been known to cause a delayed neuropathy called Organophosphorus Induced Delayed Neuropathy (OPIDN). Clinical manifestation of OPIDN is characterized by a delay period which is observed between 8 to 14 days after dosing. Toxic signs induce flaccid paralysis of lower and upper limbs and changes in neurons defined as a central-peripheral distal sensory-motor axonopathy. Although the mechanism is not clearly understood, OPs toxicity is attributed to inhibition of NTE. The initiation of OPIDN requires inhibition of NTE. Methods to elucidate mechanism of the toxicity may include use of other chemicals which can potentiate or prevent toxicity. Phenylmethylsulfonyl Fluoride (PMSF) is one such agent which has been widely utilized in mechanistic studies of OPIDN. Phenylmethylsulfonyl fluoride is a serine protease inhibitor which has been used to elucidate the mechanism of OP induced delayed neuropathy. Phenylmethylsulfonyl fluoride prevents OPIDN when given prior to an OP compound, but if PMSF is administered after an OP compound it potentiates the neurotoxicity.