Meiniel_1979_Arch.Anat.Histol.Embryol_62_29

Simple methods were applied to study the teratogenesis in Quail embryos induced by two important organophosphorous compounds: parathion and dicrotophos. Parathion led only to vertebral malformations, as other natural and synthetic cholinomimetics: nicotine, carbamylcholine, decamethonium, neostigmine... Dicrotophos induced not only vertebral malformations (specific to neuromuscular junction poisons) but also beak, legs and feather abnormalities (peripheric malformations which are also produced by insuline and sulfanilamide). Oximes and hydroxamic acids, some of these being analogs of nicotinamide, were tested as antiteratogens. The 3-(CO-NH2), or -(CO-NHOH), substituted pyridinic compounds (nicotinamide, nicotinohydroxamic acid) prevent perfectly dicrotophos-induced beak and legs malformations, in tertiary amine form, but very little in quaternary amine form (methyliodide). The 4-substituted pyridinic compound (isonicotinohydroxamic acid) and aliphatic oxo-oximes were quite ineffecient against these malformations. The vertebral malformations, as a rule, were not lessened by the compounds tested, except for isonicotinoyl-formaldoxime methyl iodide and in some degree for nicotinohydroxamic acid. From these observations, it results that teratogenesis induced by compounds as dicrotophos is rule by a plurificatorial determinism. The beak and legs malformations are prevented by analogs of nicotinamide. In the contrary, the vertebral malformations induced by parathion or dicrotophos are nicotinamide unsensitive and are only prevented by powerful cholinesterase reactivators as pralidoxime or TMB4 (MEINIEL, 1976 b) but are reduced little or not at all by less potent cholinesterase reactivators (HEATH).