Divergent effects of postmortem ambient temperature on organophosphorus- and carbamate-inhibited brain cholinesterase activity in birds

Abstract

Diagnosis of wildlife mortality from organophosphorus and carbamate pesticides is made by demonstration of critical depression (e.g., >50%) of whole brain cholinesterase (ChE) activity and detection of anti-ChE pesticide residue. In the field, this 50% criterion is usually far exceeded for organophosphorus poisonings, while ChE activity may be near normal for carbamate poisonings. Because dead wildlife may remain in the field for variable durations before collection, the temporal effect of moderate ambient temperatures on uninhibited and inhibited brain ChE was evaluated. Adult Japanese quail ( Coturnix japonica) were dosed with 0, 1, 3, or 9 mg of carbofuran or dicrotophos per kg body weight, survivors were euthanized after 1 hr, and all specimens were randomized to 18, 25, or 32°C for 0, 1, 2, or 3 days. Toxic response was dose dependent for all variables measured. Carbofuran evoked rapid response at all dosages and death within 30 min or the subject seemed to recover within 60 min, while response to dicrotophos was not pronounced for about 30 min but then persisted through time of euthanasia. Postmortem reactivation was demonstrated for carbamylated ChE while activity of phosphorylated ChE continued to decrease. Rapid inhibition and spontaneous reactivation of carbamylated enzyme explained both toxicity and postmortem changes for carbofuran treatments. Phosphorylation of ChE is a comparatively slow and essentially irreversible reaction that explains both delayed response to dicrotophos and continued depression of postmortem enzyme. Control whole brain ChE activity was resilient in intact birds exposed to above freezing temperatures to 32°C for 1 day or to 25°C for 3 days.