RESUMO
The repellent efficacies of the U.S. military repellent 33% N,N-diethyl-3-methylbenzamide (deet), 10% and 20% (1S, 2'S) 2-methylpiperidinyl-3-cyclohexene-1-carboxamide (SS220) and 10% and 20% 1-methyl-propyl-2-(hydroxyethyl)-1-piperidinecarboxylate (Bayrepel) cream formulations on human volunteers against the lone star tick Amblyomma americanum (L.) were evaluated in a simulated forest floor environment over a 12-h testing period. At 2-h intervals, volunteers, with repellent applied in a 5-cm-wide band around each ankle, stood for 5 min in plastic tubs containing leaf litter and 100 host-seeking A. americanum nymphs. Ticks were allowed to remain on a volunteer's feet and ankles for an additional 5 min after the volunteer exited the tub. All repellent formulations provided high levels of protection for the entire 12 h. No ticks crossed 5-cm-wide bands of 20% SS220 and Bayrepel during any challenge, and thus 100% protection was afforded throughout the test. These formulations showed a long-lasting efficacy hitherto unknown in tick repellents intended for use on human skin.
Assuntos
Repelentes de Insetos/farmacologia , Ixodidae/efeitos dos fármacos , Ixodidae/fisiologia , Pele/parasitologia , Administração Tópica , Adulto , Animais , Estudos Cross-Over , Cicloexenos , DEET , Relação Dose-Resposta a Droga , Feminino , Humanos , Repelentes de Insetos/administração & dosagem , Masculino , Ninfa/efeitos dos fármacos , Ninfa/fisiologia , Piperidinas , Olfato/fisiologia , Fatores de Tempo , Resultado do TratamentoRESUMO
Administration of a single oral dose of the malathion impurity, O,O,S-trimethyl phosphorothioate (OOS-Me) or O,S,S-trimethyl phosphorodithioate (OSS-Me), to the rat resulted in hemostatic disorders, e.g. prolongation of blood clotting, prothrombin and thrombin time. Deficiency of coagulation Factors II, V and VII was also observed. OOS-Me and OSS-Me also caused dose-dependent increases of beta-glucuronidase in the blood with a maximum of 15- and 31-fold observed following treatment with 60 mg/kg OOS-Me and 40 mg/kg OSS-Me, respectively. Analysis of serum beta-glucuronidase by isoelectrofocusing electrophoresis showed that the liver endoplasmic reticulum was the source of this enzyme released into the blood. Co-treatment of OOS-Me with 5% O,O,O-trimethyl phosphorothioate (OOO-Me), a potent antagonist of OOS-Me-induced delayed toxicity, prevented hemostatic disorders but had no effect in reducing beta-glucuronidase levels. However, pretreatment of rats with piperonyl butoxide reduced the amount of beta-glucuronidase released into the blood. Of other O,O,S-trialkyl phosphorothioates examined, the O,O-diethyl S-alkyl phosphorothioates showed the highest activity in increasing beta-glucuronidase levels.
Assuntos
Doença Hepática Induzida por Substâncias e Drogas , Organotiofosfatos/toxicidade , Compostos Organotiofosforados/toxicidade , Administração Oral , Alanina Transaminase/sangue , Animais , Aspartato Aminotransferases/sangue , Coagulação Sanguínea/efeitos dos fármacos , Relação Dose-Resposta a Droga , Glucuronidase/sangue , Hemostasia/efeitos dos fármacos , Fígado/enzimologia , Malation/toxicidade , Masculino , Organotiofosfatos/administração & dosagem , Organotiofosfatos/antagonistas & inibidores , Organotiofosfatos/farmacologia , Tempo de Protrombina , Ratos , Ratos Endogâmicos , Tempo de TrombinaRESUMO
O,O,S-Trimethylphosphorothioate (OOS-Me) and O,S,S-trimethylphosphorodithioate (OSS-Me) are impurities in technical grade malathion and related insecticides which have been shown to cause delayed death in rats following a single oral dose of 40-60 mg/kg. In connection with studies on the mode of action of these compounds, work on the microdissection and examination of nephrons was carried out. Nephrons from impurities-treated rats showed swelling, distortion and distension of glomeruli, as well as narrowing of the first part of the proximal tubule (swan neck). These results were similar to those observed from kidney tissue obtained from cadmium-chloride-treated rats and are indicative of OOS-Me and OSS-Me-induced kidney tubule damage.