RESUMEN
In this paper, the level of resistance to four insecticides of 3 Blatella germanica strains collected from various places in the City of Havana province was evaluated. These strains were resistant to two pyrethroids (cypermethrin and lambda-cyalothrine) and to organophosphorate malathion but susceptible to carbamate propoxur. The values of alpha and beta esterases, acetylcholinesterase and gluthatione-S-transferase were estimated in three strains involved in the study. The results of the study showed high esterase activity in all the strains, mainly beta esterases and two of the three strains presented with high gluthation-S-transferase enzyme. No changes in acetylcholinesterase were demonstrated in relation to the reference strain. The association of levels of resistance to insecticides, the possible resistance mechanisms in each strain and the results of the enzymatic activity were also analyzed.
Asunto(s)
Blattellidae/efectos de los fármacos , Proteínas de Insectos/fisiología , Resistencia a los Insecticidas , Insecticidas/farmacocinética , Administración Tópica , Animales , Blattellidae/enzimología , Blattellidae/fisiología , Inducción Enzimática , Esterasas/fisiología , Glutatión Transferasa/fisiología , Inactivación Metabólica , Resistencia a los Insecticidas/fisiología , Insecticidas/administración & dosificación , Malatión/administración & dosificación , Malatión/farmacocinética , Masculino , Nitrilos/administración & dosificación , Nitrilos/farmacocinética , Propoxur/administración & dosificación , Propoxur/farmacocinética , Piretrinas/administración & dosificación , Piretrinas/farmacocinéticaRESUMEN
The resistance mechanisms of Blatella germanica, one of the most important urban plagues worldwide since it is a mechanical vector that houses a number of highly harmful viruses, fungi, helmints and bacteria were studied. There are different control methods used against Blattella germnanica, with insecticides playing the leading role. Their uncontrolled application has caused the development of insecticice resistance in this species. This paper adapted biochemical methods to detect the enzymes esterase, acetylcholinesterase and glutathine-S-transferase as posible resistance mechanisms. To this end, all the parameters that allow finding out if a strain is susceptible or resistant to each mechanism were set.
Asunto(s)
Acetilcolinesterasa/análisis , Blattellidae/enzimología , Esterasas/análisis , Glutatión Transferasa/análisis , Inactivación Metabólica/fisiología , Proteínas de Insectos/análisis , Resistencia a los Insecticidas/fisiología , Insecticidas/farmacocinética , Acetilcolinesterasa/genética , Acetilcolinesterasa/fisiología , Animales , Bioensayo , Blattellidae/efectos de los fármacos , Blattellidae/genética , Inhibidores de la Colinesterasa/farmacología , Compuestos Cromogénicos , Relación Dosis-Respuesta a Droga , Activación Enzimática , Esterasas/genética , Esterasas/fisiología , Frecuencia de los Genes , Genes de Insecto , Glutatión Transferasa/genética , Glutatión Transferasa/fisiología , Inactivación Metabólica/genética , Proteínas de Insectos/genética , Proteínas de Insectos/fisiología , Resistencia a los Insecticidas/genética , Insecticidas/clasificación , Propoxur/farmacocinética , Reproducibilidad de los Resultados , Especificidad por SustratoRESUMEN
Effects of the synergists piperonyl butoxide (PBO) and S,S,S-tributyl phosphorotrithioate (DEF) on propoxur pharmacokinetics were examined in the German cockroach, Blattella germanica (L.). Treatment of adult male German cockroaches with the cytochrome P450 monooxygenase inhibitor, PBO, or the esterase inhibitor, DEF, increased propoxur toxicity by 2- and 6.8-fold, respectively, implicating hydrolysis as a major detoxification route of propoxur in the German cockroach. However, significant hydrolytic metabolism could not be demonstrated conclusively in vitro resulting in a conflict between in situ bioassay data and in vitro metabolic studies. In vitro propoxur metabolism with NADPH-fortified microsomes produced at least nine metabolites. Formation of metabolites was NADPH-dependent; no quantifiable metabolism was detected with cytosolic fractions. However, microsomal fractions lacking an NADPH source did produce a low, but detectable, quantity of metabolites (1.6 pmol). PBO inhibited NADPH-dependent propoxur metabolism in a dose-dependent fashion, implicating cytochrome P450 monooxygenases as the enzyme system responsible for the metabolism. Interestingly, DEF also inhibited the NADPH-dependent metabolism of propoxur, albeit to a lower extent. Treatment with PBO or DEF also caused a significant reduction in the cuticular penetration rate of propoxur. The data demonstrate that unanticipated effects are possible with synergists and that caution must be exercised when interpreting synergist results.