FIELD RESULTS USING CHOLINESTERASE REACTIVATION TECHNIQUES TO DIAGNOSE ACUTE ANTICHOLINESTERASE POISONING IN BIRDS AND FISH

Authors
Citation
W. Stansley, FIELD RESULTS USING CHOLINESTERASE REACTIVATION TECHNIQUES TO DIAGNOSE ACUTE ANTICHOLINESTERASE POISONING IN BIRDS AND FISH, Archives of environmental contamination and toxicology, 25(3), 1993, pp. 315-321
Citations number
29
Categorie Soggetti
Toxicology,"Environmental Sciences
ISSN journal
00904341
Volume
25
Issue
3
Year of publication
1993
Pages
315 - 321
Database
ISI
SICI code
0090-4341(1993)25:3<315:FRUCRT>2.0.ZU;2-E
Abstract
The inhibition of brain cholinesterase (ChE) activity in organophospha te (OP)- or carbamate (CB)-poisoned animals is usually determined by c omparison with the normal activity in control specimens. Alternatively , the activity of pesticide-inhibited ChE can be restored, ideally up to normal levels, using simple in vitro procedures, thereby providing a reference value against which ChE inhibition can be estimated. The a ctivity of phosphorylated ChE can be increased by the addition of the nucleophilic reagent pyridine 2-aldoxime methiodide (2-PAM), while the spontaneous reactivation of carbamylated ChE can be enhanced by dilut ion. These procedures can also be used to differentially diagnose OP a nd CB poisoning. Brain ChE inhibition in birds and fish from field poi soning incidents was determined using reactivation techniques and norm al activity data from separate control specimens. In OP-poisoned birds , the mean inhibition relative to 2-PAM-treated samples and controls r anged from 77-82% and 84-87%, respectively. The corresponding values f or OP-poisoned fish were 48-82% and 66-86%, respectively. In CB-poison ed birds, the mean inhibition relative to diluted samples and controls ranged from 22-56% and 33-76%, respectively. The reactivation of carb amylated ChE was further enhanced by increasing the dilution ratio and lengthening the incubation period. Although ChE activity was not full y restored to normal levels in many individuals, diagnostically signif icant inhibition was demonstrated in most cases. In OP-poisoned fish h eld 24 h postmortem at 20-degrees-C, 2-PAM restored brain ChE activity to that of similarly handled, unexposed controls. After postmortem st orage for 48 h, ChE activities in reactivated and inhibited samples we re statistically indistinguishable due to the aging of the phosphoryla ted ChE. Despite the limitations imposed by aging, ChE reactivation is a potentially useful diagnostic technique, particularly when control data are unavailable or difficult to obtain.