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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Study of delayed neurotoxicity caused by fatty acid anilides in hens.

We have observed that the oral administration of a single dose of a mixture of oleyl and linoleylanilides (80 mg/kg) in adult hens determines the apparition of delayed muscular neuropathy, which we have compared to that induced by metamidophos as a model of organophosphate-induced delayed neuropathy (OPIDN). We have compared the modifications produced by each of the 2 treatments on the enzymatic activity of neuropathy target esterase ( NTE) measured in nervous tissue homogenates of brain, medulla and sciatic nerve. In addition we determined total esterases (TE), acetylcholine esterase (AchE) and serum creatine phosphate kinase (CPK). The organophosphate compound (OP) induced an initial reduction in the activity of NTE, TE and AchE which was reestablished 48 h later, except for brain TE which increased slowly during the latency period. This behaviour was accompanied by a permanent increase in the activity of serum CPK. Anilides induced a strong activation of AchE, NTE and TE (except brain TE) in the first 24-36 h. Normal levels were relatively quickly reestablished in brain (by 48 h) and slowly in medulla and sciatic nerve. But the AchE activity remained high throughout the whole period of latency. This activity level coincided with the AchE level observed at the onset of signs in animals dosed with OPs. CPK was also increased in sciatic nerve at 15 d but was depressed in serum throughout the whole latency period. Substances with chemical characteristics very different from OPs can induce a delayed neuropathy with modification of the activity of NTE.[1]


  1. Study of delayed neurotoxicity caused by fatty acid anilides in hens. Sanz, P., Moreno, E., Blasco, R., Repetto, M. Veterinary and human toxicology. (1990) [Pubmed]
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