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A 76-year old farmer ingested 100 g of chlorphenamidine (Galectron), a plant acaricle, for the purpose of suicide. Gastric lavage was performed and the patient survived. Methemoglobinemia was noted after emergency treatment and was still present at 20 hours after ingestion of the compound. The patient was lethargic for at least 50 hours. Moderate neutrophilic leukocytosis and kidney injury were observed.
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The aim of this work was to learn the toxicity of acaricides: monocrotophos, chlorobenzilate and chlorphenamidine when used as an immersion and as a spray on the phytophagous mites, Tetranychus (T) urticae, Tetranychus (T) cinnabarinus and Tetranychus (T) ludeni under laboratory conditions. It was concluded that the mite T. urticae was sensitive to chlorphenamidine at least when used as a spray without killing them in a significant level. However the mites T. cinnabarinus and T. ludeni were sensitive to chlorphenamidine when using immersion method. The monocrotophos and the chlorobenzilate were toxic of the three species of mites using though the employed methods.
An outbreak of hematuria occurred from May 20 to May 23, 1975, among employees of a chemical packaging plant. Nine of 22 workers who packaged the insecticide chlordimeform in a separate shed became severely ill with abdominal pain, dysuria, urgency to void, or hematuria. None of 18 persons who worked in other areas of the plant were affected. Four additional workers who had packaged the chemical during the previous year had a history of similar symptoms. Bladder biopsy specimens from three affected persons showed severe hemorrhagic cystitis; chlordimeform and 2-methyl-4-chloroaniline, a metabolite of chlordimeform, were present in urine specimens collected three days after exposure. The illness lasted from one week to two months; the workers recovered completely. Chlordimeform that was injected subcutaneously into three cats produced similar, though less severe, changes in the bladders of two animals.
Chlordimeform N'-(4-choro-O-tolyl)-N,N-dimethyl-formamidine; CDF), an acaracide-insecticide, relaxed helically cut strips of rabbit thoracic aorta and deadventitiated aorta strips. Relaxations by CDF of aorta strips contracted by 5 x 10(-7) M prostaglandin F2 alpha were not altered by the antimuscarinic agent atropine (10(-5) M), the beta-adrenergic antagonist propranolol (10(-5) M), the histamine H2 antagonist cimetidine (2 x 10(-4) M), the dopamine antagonist haloperidol (10(-5) M) or the Na+-K+-ATPase inhibitor ouabain (5 x 10(-6) M). CDF further relaxed deadventitiated strips contracted by 10(-6) M NE or 40 mM potassium and then partially relaxed by 10(-5) M verapamil. CDF (10(-5) M) potentiated contractions caused by the addition of calcium to potassium depolarized strips in zero calcium media, but higher concentrations reduced calcium-induced contractions. The highest CDF concentration (10(-2) M) not only prevented tension increase on calcium addition, but also progressively decreased tension to below baseline levels. The addition of 10(-2) M CDF to aorta strips not contracted by a vasoactive agent decreased resting tension. This relaxation was usually maximal at 10(-3) M and less at 10(-2) M. Thus, CDF relaxes vascular smooth muscle, not by antagonism at the usual vascular relaxant receptors, but by interference with calcium utilization.
Octopamine and an agonist, chlordimeform, increase the responsiveness of adult and pharate adult Manduca sexta to gentle mechanical stimulation of the wing. Higher doses of chlordimeform elicit almost continuous production of the flight motor pattern in both adults and pharate adults, and the effect persists for more than 24 h. The dose of chlordimeform necessary for this effect increases with age. Mechanical stimulation of the wing of pharate adults elicits several cycles of flight motor pattern, but with repeated stimulation the animal habituates. Habituation is slower in chlordimeform-treated animals than in controls. Injection of octopamine (1-8 X 10(-8) mol) or chlordimeform (3 X 10(-9) mol) into the mesothoracic ganglion elicits the flight motor pattern. The excitatory actions of both compounds can be blocked by cyproheptidine. Chlordimeform (5 X 10(-8) mol) in acetone applied to the wing does not cause a noticeably greater increase in teh electrical activity of sensory neurons than does acetone applied alone; this result suggests that chlordimeform does not act on these peripheral sites or on axonal membranes in general. We suggest that chlordimeform and octopamine act on the thoracic ganglia to alter the level of excitation or effectiveness of synaptic transmission among central neurons, including those involved in producing the flight motor pattern.
The information available concerning the effects of compounds utilized as pesticides on functions of the reticuloendothelial system is quite limited. Review of selected examples of such studies in this and other reports (3) reveals considerable diversity in terms of species of experimental animal, purity and dose of pesticide, length of exposure, and class of pesticide employed. Observations include depression, enhancement, or no significant effect on the selected reticuloendothelial system function studies. With the present available information it is difficult to formulate general conclusions or to predict whether or not any individual pesticide will consistently and significantly alter any specific function of the reticuloendothelial system. At the present time, it is not known if pesticides within a single chemical class act in a similar manner in regard to their ability to influence reticuloendothelial system function. In addition, the relationship, if any, between the toxic, mutagenic teratogenic, or carcinogenic potential of any pesticide and its ability to alter the reticuloendothelial system is also unknown. More extensive systematic studies in experimental animal models would appear to be required before protocols to effectively evaluate the potential of pesticides to influence reticuloendothelial system function in man can be developed.
Chlordimeform (N'(4-chloro-o-tolyl)-N, N-dimethylformamidine; CDM) is a formamidine insecticide acaricide whose major active metabolite is its N-monomethyl analog, desmethylchlordimeform, (DCDM). While their pesticidal action in invertebrates appears to be related to activation of octopamine receptors, their mechanism of action in mammals has not been established. Because of similarities between octopamine and adrenergic receptors and suggestions of CDM and DCDM action on adrenoceptors, the in vitro interactions of CDM and DCDM with adrenoceptors were studied. In mouse brain membrane preparations CDM inhibited the binding of [3H]-clonidine to alpha 2- adrenoceptors and of [3H]-WB4101 to alpha 1-adrenoceptors with IC50 values of 18.2 and 87 microM, respectively. DCDM was a much more potent inhibitor, with IC50 values toward alpha 2-, and alpha 1-adrenoceptors of 44 nM and 1 microM, respectively. Both compounds were only weak inhibitors of the binding of [3H]-dihydroalprenolol to beta-adrenoceptors and of [3H]-quinuclidinyl benzilate to muscarinic receptors and were inactive toward benzodiazepines and gamma aminobutyric acid (GABAA) receptors. Inhibition of [3H]-clonidine binding by both compounds was competitive, as indicated by a decreased receptor affinity without changes in receptor density. Interaction of CDM and DCDM with [3H]-WB4101 binding, on the other hand, was more complex, and not of the competitive type. These results show that CDM and its metabolite DCDM can interact directly in vitro with alpha-adrenergic receptors, suggesting that these receptors could mediate some of the effects of CDM and DCDM in vivo.
Low doses of the formamidine pesticide, chlordimeform (CDM) induce voracious daytime feeding in non-food deprived rats. Following CDM (10 mg/kg), food intakes were five times control intakes after 3 h and 1.1 times control intakes after 24 h. Other selected formamidines, such as the N-demethylated metabolite of CDM, and amitraz, increased 3-h food intake by two and five times control intake, respectively. Anorexia accompanied by excessive CNS stimulation was noted with higher doses of CDM (above 40 mg/kg) and other formamidines. This contrasts with the sedation usually observed with high doses of other structurally diverse appetite stimulants. In addition, hyperphagia was not observed with other CNS stimulants or local anesthetics such as amphetamine, cocaine, and holocaine. Thus the formamidines constitute a new class of appetite stimulants, which should prove to be useful agents for the study of feeding behavior.