“…Larvae scored as malformed, showed often gross alterations in the tail flexure coupled with a great decrease of neuromuscular activity, and these results are well comparable to those of other authors (Snawder and Chambers, 1989;Vismara et al, 1996;Richards and Kendall, 2002). It is well known that in non-target organisms, such as amphibians, fishes, birds and mammals, AChE inhibition is the primary manifestation of toxicity during OP exposure (Thomson et al, 1991;Sultatos, 1994;Calumpang et al, 1997;Fulton and Key, 2001) and that OP compounds produce typical signs of anti-cholinesterase toxicity such as complex posturing movements, body shaking or skeletal muscle fasciculation associated with muscle fibre damages in mammals (Gupta et al, 1987;Karalliedde and Henry, 1993;De Bleecker et al, 1994;John et al, 2003). The abnormal tail flexure observed in CPFs and MTNs could be the consequence of the cholinergic phase, where the AChE inhibition causes repetitive firing of muscle fibres leading to the axis tail folding and, at high concentrations, to paralysis.…”