Inhibitor Report for: Dicrotophos

Brain and plasma cholinesterase (ChE) activities were determined for mallard ducklings (Anas platyrhynchos) exposed to dicrotophos and fenthion. Recovery rates of brain ChE did not differ between ducklings administered a single oral dose vs. a 2-week dietary dose of these organophosphates. Exposure to the organophosphates, followed by recovery of brain ChE, did not significantly affect the degree of brain ChE inhibition or the recovery of ChE activity at a subsequent exposure. Recovery of brain ChE activity followed the general model Y = a + b(logX) with rapid recovery to about 50% of normal, followed by a slower rate of recovery until normal ChE activity levels were attained. Fenthion and dicrotophos-inhibited brain ChE were only slightly reactivated in vitro by pyridine-2-aldoxime methiodide, which suggested that spontaneous reactivation was not a primary method of recovery of ChE activity. Recovery of brain ChE activity can be modeled for interpretation of sublethal inhibition of brain ChE activities in wild birds following environmental applications of organophosphates. Plasma ChE activity is inferior to brain ChE activity for environmental monitoring, because of its rapid recovery and large degree of variation among individuals.

A series of in vitro trials using unfed larvae and fully fed adult ticks confirmed ixodicidal resistance in the one-host Pantropical Blue Tick, Boophilus microplus (Canestrini). Fifty-seven of 64 field isolates were resistant to arsenic; 10 of 56 were resistant to toxaphene; 1 of 5 were resistant to lindane; 3 of 5 were resistant to dieldrin; 3 of 19 were resistant to DDT and 8 of 55 were resistant to the organophosphorus ixodicide, dioxathion. One of the field isolates resistant to dioxathion was also highly resistant to the carbamate, carbaryl, and to the organophosphorus ixodicides benoxophos and diazinon. A second was resistant to the organophosphorus ixodicides benoxophos, diazinon, carbophenothion, dicrotophos, ethion, fenitrothion and quintiofos. Low levels of resistance, less than 3X, were shown to chlorfenvinphos and coumaphos. No resistance was shown to chlorpyrifos, bromophos ethyl or the diamidine ixodicide, amitraz. In hand-spraying trials no variation in the susceptibility of an organophosphorus resistant strain or the susceptible laboratory strain to amitraz was observed. This is the first recorded resistance to ixodicides by B. microplus in Africa.

Ten day old chick sympathetic ganglia cultured in a microslide assembly were treated with a selected group of organophosphate pesticides to evaluate their cytotoxicity ranges, and the usefulness of such a model for screening pesticides. Examination by phase contrast and light microscopy for chemically-induced morphological alteration of nerve fibers, glial cells and neurons provided the criteria for quantitation and assessment of the toxic effects. Concentrations that produced half-maximal effects ranged from 1 x 10(-6)M (severely toxic) for methylparathian, diazinon, paraoxon, mevinphos, diisopropylfluorophosphate, tri-o-tolyl phosphate and its mixed isomers to a 1 x 10(-3)M (intermediate) for malathion, leptophos, coumaphos, mono- and dicrotophos. Some or no effects were evident at 1 x 10(2-)M for O'ethyl-O-p-nitrophenyl phenyl phosphonothioate, tri-m-tolylphosphate, chlorpyriphos and triphenyl phosphate. In all instances, nerve fibers were more sensitive than neurons or glial cells to insecticides. All cellular growth was inhibited at 1 x 10(-2)M (except triphenyl phosphate). Below 1 x 10(-7)M, no inhibitory effects were evident. The secondary abnormalities included decreased cellular migration, diffuse cellular growth pattern, increased vacuolization, nerve fiber swelling and cellular degeneration. The cytotoxic effects of these chemicals do not appear to be related to in vivo toxicity or cholinesterase inhibition potential.