Organophosphorus pesticides are widely used as insecticides in agriculture both in developed and developing countries in spite of reported poten­tial toxicity. They induce neurotoxic effects either upon acute or chronic exposure. It was found previously that zinc (Zn) supplementation exerted a neuroprotective effect against organophosphorus pesticide-induced neurodegenerative disorders in experimental animals. This study therefore, aimed to investigate the possible association between serum zinc level and organophosphorus-induced delayed polyneuropathy. Fifty acute organophosphorus poisoned cases admitted to Zagazig University Hospitals from February to August 2016 were enrolled in this study. Another Forty six healthy individuals (age- and sex-matched) served as a control group. Both groups were investigated for serum lipid peroxidation product (malondialdehyde: MDA) and total antioxidant capacity (TAC) levels as well as lymphocytic neuropathy target esterase (NTE) and plasma acetylcholinesterase (AChE). Then, they were followed up for 4 weeks to assess the development of delayed polyneuropathy (diagnosed clinically and confirmed by motor and sensory conduction studies). Serum levels of Zn, MDA and TAC as well as lymphocytic NTE and plasma AChE were measured for those developed organophosphorus delayed polyneuropathy. Organophosphorus intoxication has resulted in a significant elevation in the levels of MDA, suggesting oxidative stress. On the other hand, TAC levels as well as measured lymphocytic NTE and plasma AChE activities were found to be significantly reduced in the intoxicated group. However, at the end of the follow up period, 7 cases developed delayed polyneuropathy; 5 of them were Zn deficient while the rest were with normal Zn level. Cases with delayed polyneuropthy showed also a significant increase in lipid peroxidation along with impairment of estrases activities compared to cases on admission. Furthermore, serum Zn level showed a significant positive correlation with TAC, AChE, NTE and a negative correlation with MDA, where serum zinc level seems to be the strongest determinants for the prediction of delayed polyneuropathy. Thus, we conclude that Zn deficiency has a potential role in organophosphorus -induced delayed polyneuropathy. This may be due to its involvement in the activity of antioxidant enzymes. However, further future large scale studies are needed to clarify the exact mechanism by which Zn deficiency mediated neurotoxicity upon organophosphorus induced polyneuropathy.