Prolonged mosquitocidal activity of Siparuna guianensis essential oil encapsulated in chitosan nanoparticles.

BACKGROUND: The use of synthetic insecticides is one of the most common strategies for controlling disease vectors such as mosquitos. However, their overuse can result in serious risks to human health, to the environment, as well as to the selection of insecticidal resistant insect strains. The development of efficient and eco-friendly insect control is urgent, and essential oils have been presented as potential alternatives to synthetic insecticides. Moreover, nanoencapsulation techniques can enhance their efficiency by protecting from degradation and providing a controlled release rate. RESULTS: We assessed the potential of chitosan nanoparticles in encapsulating Siparuna guianensis essential oil, and maintaining its efficiency and prolonging its activity for the control of Aedes aegypti larvae. The encapsulation was characterized by scanning electron microscopy (SEM), Fourier-transform infrared spectroscopy (FTIR), and thermogravimetric analysis (TGA), with an encapsulation efficiency ranging from 84.8% to 88.0%. Toxicity studies have demonstrated efficacy against mosquito larvae over 50% for 19 days with 100% mortality during the first week. This persistent action is presumably due to the enhanced contact and slow and maintained release conferred by chitosan nanoparticles. Furthermore, the exposure of aquatic non-target organisms (e.g. embryos and small adult fishes) revealed adequate selectivity of these nanoparticles. CONCLUSIONS: The encapsulation of S. guianensis essential oil in chitosan nanoparticles showed promising potential as a larvicide control alternative and should be considered within strategies for fighting Ae. aegypti.

The NF kappa B-mediated control of RS and JNK signaling in vitamin A-treated cells: duration of JNK-AP-1 pathway activation may determine cell death or proliferation.

Nuclear factor kappa B (NFkappaB) has emerged as a crucial regulator of cell survival, playing important functions in cellular resistance to oxidants and chemotherapeutic agents. Recent studies showed that NFkappaB mediates cell survival through suppression of the accumulation of reactive species (RS) and a control of sustained activation of the Jun-N-terminal kinase (JNK) cascade. This work was undertaken in order to evaluate the role of NFkappaB in modulating the pro-oxidant effects of supplementation with vitamin A (retinol, ROH) in Sertoli cells, a major ROH physiological target. In this work, we reported that ROH treatment increases mitochondrial RS formation leading to a redox-dependent activation of NFkappaB. NFkappaB activation played a pivotal role in counteract RS accumulation in ROH-treated cells, since NFkappaB inhibition with DNA decoy oligonucleotides or pharmacological inhibitors (BAY-117082) potentiated ROH-induced RS accumulation and oxidative damage. In the presence of NFkappaB inhibition, ROH-induced oxidative stress promoted a prolonged activation of the JNK-activator protein 1 (AP-1) pathway and induced significant decreases in cell viability. Inhibition of JNK-AP-1 with decoy oligonucleotides to AP-1 or JNK inhibitor SP600125 prevented the decreases in cell viability. Antioxidants blocked the persistent JNK-AP-1 activation, cell oxidative damage, and the decreases in cell viability induced by NFkappaB inhibition. Finally, our data point superoxide dismutase (SOD)2 as a potential antioxidant factor involved in NFkappaB protective effects against ROH-induced oxidative stress. Taken together, data presented here show that NFkappaB mediates cellular resistance to the pro-oxidant effects of vitamin A by inhibiting RS accumulation and the persistent and redox-dependent activation of JNK-AP-1 cascade.