These findings are the first collective report of human plasma, erythrocyte, and whole blood cholinesterase activities as determined by the modified electrometric method, and they could serve as reference points for future studies that involve human exposure to anticholinesterase pesticides.

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The present study was undertaken to examine the acute toxicity (LD50) and neurobehavioral manifestations in the open-field activity and tonic immobility tests in 7-14 day-old chicks treated with the H1-receptor antagonist diphenhydramine. Plasma and whole brain cholinesterase activities were also determined in the chicks. The LD50 of diphenhydramine in chicks was 49.3 mg/kg, intramuscularly (i.m.). The signs of diphenhydramine toxicosis in the chicks which appeared within one hour after injection included excitation, jumping, whole body tremor, ataxia, gasping, frequent defecation, paralysis and recumbency. Fifteen minutes after i.m. injection, diphenhydramine at 2.5 and 5 mg/kg decreased the general locomotor activity of the chicks in the 5-min open-field activity test, as seen by a significant increase in the latency to move from the center of the open-field arena and decreases in the numbers of lines crossed and escape jumps in comparison with control values. Diphenhydramine significantly decreased the frequencies of pecking and defecation only at 5 mg/kg when compared with respective control values. Diphenhydramine treatments at 2.5 and 5 mg/kg also significantly increased the durations of tonic immobility of the chicks and decreased their whole brain cholinesterase activity by 33 and 30%, respectively, in comparison with the control values. In conclusion, the data suggest that diphenhydramine induces central nervous system depression in chicks at doses below the LD50 value of the drug which is reported here for the first time.

Acute toxic effects of three commonly used insecticidal preparations of the organophosphates chlorpyrifos, diazinon, and dichlorvos were examined in mixed breed broiler chicks, and cholinesterase activity in plasma and brain were measured. The acute (24 h) oral median lethal doses (LD 50 ) of chlorpyrifos, diazinon, and dichlorvos were 10.79 mg kg -1 , 6.32 mg kg -1 , and 6.30 mg kg -1 , respectively, as determined by the up-and-down method in chicks. Signs of cholinergic toxicosis in the chicks appeared within two hours after dosing, and they included salivation, lacrimation, gasping, frequent defecation, drooping of wings, tremors, convulsions, and recumbency before death. Halving the oral LD 50 of chlorpyrifos (5 mg kg ) caused immobility and wing drooping, but not the clinical signs of cholinergic toxicity. However, at full LD 50 doses of these insecticides, chicks showed clinical signs of cholinergic toxicity similar to those seen in the LD 50 experiments. Two out of six chicks died within two hours after treatment with LD 50 doses of chlorpyrifos and dichlorvos, whereas LD 50 dosing with diazinon caused death in three out of six chicks. Compared to control values, the insecticides reduced plasma and whole brain cholinesterase activities by 29 % to 84 % and 18 % to 77 %, respectively, depending on the dose. The decrease in plasma cholinesterase correlated well (r = 0.82) with that of the brain. These data suggest that organophosphate insecticides administered orally at LD 50 doses induce clinical signs of cholinergic poisoning and concurrently reduce brain and plasma cholinesterase activities in chicks.

Plasma and erythrocyte cholinesterase (ChE) activities of male farm workers exposed to pesticides during their routine work were lower than those of unexposed control subjects by 14 and 4%, respectively. Diphenhydramine and Carbaryl inhibited plasma and erythrocyte ChE activities in vitro in pesticide-exposed and unexposed subjects. The percentages of in vitro ChE inhibition induced by carbaryl in the plasma and erythrocytes of unexposed controls ranged between 47-85% and 19-47%, respectively, whereas they were 35-60% and 3-12% in the pesticide-exposed group, respectively. In vitro pretreatment of plasma and erythrocyte ChE with diphenhydramine (20 μM) significantly reduced the inhibitory effect of carbaryl (10 μM) on them by 18% and 10%, respectively. In conclusion, subjects exposed to pesticides during their routine work in agriculture are at risk of reduced blood ChE activity. Diphenhydramine appeared to partially protect blood ChE in vitro from additional carbaryl-induced enzyme inhibition in both pesticide-exposed and unexposed subjects.

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Summary The sedative effect of medetomidine was evaluated in 6 male Awassi sheep. Medetomidine at 40 μg/kg, i.m. induced sedation and recumbency in the sheep within 9±1 and 17±4 minutes, respectively. The duration of recumbency was 58 ± 1 minutes. Medetomidine produced good analgesia and marked muscle relaxation in the recumbent animals for 30 to 45 minutes. The side effects of medetomidine were bradycardia, respiratory depression, stasis of the rumen with tympany, salivation and polyuria. The animals recovered from the sedative and side effects of medetomidine 1.5 to 2 hours after gaining the righting reflex without any apparent adverse effect. The results suggested that medetomidine could be a useful sedative analgesic in sheep.

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