The control of fall armyworm (Spodoptera frugiperda) populations involves the application of pesticides that cause several unwanted effects to humans and other animals, as well as to environment. Sodium chloride (NaCl) has been used in agriculture to potentiate the toxicity of pesticides. Here, the effects of NaCl on the viability of eggs, larvae, and pupae, as well as on development of S. frugiperda were evaluated. The treatment with 0.15 M NaCl caused a 35% reduction of egg hatching and the ingestion of artificial diet containing the salt caused mortality of caterpillars, pre-pupae, and pupae, as well as delayed the development of the insects. The larval, pre-pupa and pupa stages were elongated by about 2, 1 and 0.8 days, respectively. Additionally, significant reduction in pupae body weight was recorded in groups treated with NaCl at 0.62 mg/g and 3.12 mg/g. Despite these effects, NaCl ingestion did not affect the viability of adults and their reproductive performance. Food deterrent assay revealed that the salt acted as a phagostimulant agent. In conclusion, NaCl reduces the hatching of S. frugiperda eggs and damage the survival of carterpillars and pupae, as well interferes with insect development.
Trypanosoma cruzi causes the lethal Chagas disease, which is endemic in Latin America. Flowers of Moringa oleifera (Moringaceae) express a trypsin inhibitor (MoFTI) whose toxicity to T. cruzi trypomastigotes was previously reported. Here, we studied the effects of MoFTI on the viability of human peripheral blood mononuclear cells (PBMCs) as well as on the production of cytokines and nitric oxide (NO) by T. cruzi-infected PBMCs. Incubation with MoFTI (trypsin inhibitory activity: 62 U/mg) led to lysis of trypomastigotes (LC50 of 43.5 µg/mL) but did not affect the viability of PBMCs when tested at concentrations up to 500 µg/mL. A selectivity index > 11.48 was determined. When T. cruzi-infected PBMCs were treated with MoFTI (43.5 or 87.0 µg/mL), the release of the pro-inflammatory cytokine TNF-α and INF-γ, as well as of NO, was stimulated. The release of the anti-inflammatory cytokine IL-10 also increased. In conclusion, the toxicity to T. cruzi and the production of IL-10 by infected PBMCs treated with MoFTI suggest that this molecule may be able to control parasitemia while regulating the inflammation, preventing the progress of Chagas disease. The data reported here stimulate future investigations concerning the in vivo effects of MoFTI on immune response in Chagas disease.
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