Abstract

Diisopropyl phosphorofluoridate (DFP) produces delayed neurotoxicity (OPIDN) in hens that is characterized by peripheral and central axonal degeneration. DFP administration resulted in mCANP activity inhibition in sciatic nerve and significant decrease in total NF-H, phosphorylated NF-H, vimentin, GFAP, tubulin, and tau. The degradation of cytoskeletal proteins even in the presence of decreased CANP activity may be ascribed to the release of intracellular Ca 2+, elevation of other proteinase activity, or modification of cytoskeletal proteins resulting in their increased susceptibility in OPIDN.

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