ABSTRACT
The prevention of Chagas disease is based primarily on the chemical control of Triatoma infestans (Klug) using pyrethroid insecticides. However, high resistance levels, correlated with control failures, have been detected in Argentina and Bolivia. A previous study at our laboratory found that imidacloprid could serve as an alternative to pyrethroid insecticides. We studied the delayed toxicity of imidacloprid and the influence of the blood feeding condition of the insect on the toxicity of this insecticide; we also studied the effectiveness of various commercial imidacloprid formulations against a pyrethroid-resistant T. infestans population from the Gran Chaco ecoregion. Variations in the toxic effects of imidacloprid were not observed up to 72 h after exposure and were not found to depend on the blood feeding condition of susceptible and resistant individuals. Of the three different studied formulations of imidacloprid on glass and filter paper, only the spot-on formulation was effective. This formulation was applied to pigeons at doses of 1, 5, 20 and 40 mg/bird. The nymphs that fed on pigeons treated with 20 mg or 40 mg of the formulation showed a higher mortality rate than the control group one day and seven days post-treatment (p < 0.01). A spot-on formulation of imidacloprid was effective against pyrethroid-resistant T. infestans populations at the laboratory level.
Subject(s)
Animals , Insect Vectors , Imidazoles/pharmacology , Insecticides/pharmacology , Nitro Compounds/pharmacology , Pyrethrins/pharmacology , Triatoma/drug effects , Argentina , Bolivia , Chagas Disease/prevention & control , Chagas Disease/transmission , Columbidae/parasitology , Feeding Behavior , Insecticide Resistance , Imidazoles/chemistry , Insect Vectors/metabolism , Insecticides/chemistry , Nitro Compounds/chemistry , Nymph/drug effects , Triatoma/classification , Triatoma/metabolismABSTRACT
Nitro-fatty acids are formed and detected in human plasma, cell membranes, and tissue, modulating metabolic as well as inflammatory signaling pathways. Here we discuss the mechanisms of nitro-fatty acid formation as well as their key chemical and biochemical properties. The electrophilic properties of nitro-fatty acids to activate anti-inflammatory signaling pathways are discussed in detail. A critical issue is the influence of nitroarachidonic acid on prostaglandin endoperoxide H synthases, redirecting arachidonic acid metabolism and signaling. We also analyze in vivo data supporting nitro-fatty acids as promising pharmacological tools to prevent inflammatory diseases.
Subject(s)
Humans , Anti-Inflammatory Agents/metabolism , Arachidonic Acid/metabolism , Fatty Acids/biosynthesis , Nitric Oxide/metabolism , Nitro Compounds/metabolism , Signal Transduction/physiology , Anti-Inflammatory Agents/chemistry , Fatty Acids/chemistry , Heme Oxygenase-1/metabolism , NADPH Oxidases/metabolism , /metabolism , NF-kappa B/metabolism , Nitro Compounds/chemistry , Peroxisome Proliferator-Activated Receptors/metabolism , Prostaglandin-Endoperoxide Synthases/metabolismABSTRACT
Reaction of 2-chloro-3,5-dinitropyridine, 2-chloro-1,3,5- trinitrobenzene and 2-chloro-1,3-dinitrobenzene with morpholine in methanol was studied spectrophotometrically at five different temperatures and the activation parameters were calculated. The results revealed that the reactions obeyed second-order kinetics and no measurable catalysis by the amine was observed. Activation of the aza group compared to ortho nitro group in the titled reaction was explained