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The Aedes aegypti mosquito is a vector of several diseases, such as dengue, malaria and the Zika virus. Synthetic insecticides such as chlorpyrifos and chlorothalonil have been used for plague control, despite causing damage to the environment and to humans. It is therefore important to study natural active compounds with a low environmental impact. The present paper developed an environmentally friendly formulation of silk fibroin (SF) associated with fatty acid esters [ethyl (FAEE-SF), propyl (FAPE-SF) and butyl (FABE-SF)] from Astrocaryum murumuru Mart. fat, which was effective against Aedes aegypti 3th instar larvae. The FABE-SF nanoemulsion induced a higher mortality rate in the larvae of the A. aegypti after 48 h (LC50 = 18.92 µg / mL). The stabilities of the nanoemulsions were monitored for 21 days, and FABE-SF exhibited greater stability throughout the monitored period, with average particle, zeta and PDI values of around 217 ± 0.85 nm, -25.6 ± 3.24 mV and 0.338 ± 0.01, respectively. This paper reported the first effective action of fatty acid esters from A. murumuru Mart. associated with silk fibroin against A. aegypti. The FABE-SF solution also had a low hemolytic index, suggesting that treatment may be safe for animal and human use.

This paper report the use of Carapa guianensis Abul. (Meliaceae) oil and derivates [fatty acid ethyl ester (FAEE’s) and free fatty acid (FFA’s)] associate with silk fibroin (SF), and its activity against the larvae of the vector Aedes aegypti. The emulsions FFA2-SF derived from AO2, that mostly contained unsaturated fatty acids, presented the best results against the larvae of Ae. aegypti after a 48 h period (LC50 = 16.79 mg.mL−1), causing structural alterations to the vector. It is suggested that the biopolymeric matrix of silk fibroin increases the biodistribution and bioavailability of active in medium aqueous. This is the first work of its type which has pointed larvicidal activity of the free fatty acid from C. guianensis, associate with silk fibroin against Aedes aegypti.

The Aedes aegypti mosquito is a vector that causes various diseases such as chikungunya fever, dengue and Zika, and therefore constitutes a public health problem. The present study was carried out to evaluate the larvicidal activity of different crude extracts (methanolic, hydroethanolic and hexanic) from leaves of Acmella oleracea solubilized in fibroin solution, as an alternative to the organic solvents that are used against Aedes aegypti. Using the Probit analysis, the hexane extract showed LC50 of 2.23 μg/mL after 24 h, whereas the hydroethanolic and the methanolic extracts showed LC50 of 28.42 μg/mL and 39.67 μg/mL, respectively. These extracts also did not show toxicity towards Chlorella vulgaris after 30 days, which suggests that they can be used without causing environmental damage. Thus, A. oleracea extract dissolved in fibroin solution could be an alternative for controlling Ae. aegypti without causing damage to the environment.

The higher resistance of stationary-phase Saccharomyces cerevisiae to H2O2 when compared with exponential phase is well characterized, but the molecular mechanisms underlying it remain mostly unknown. By applying the steady-state H2O2-delivery model, we show that (a) cellular permeability to H2O2 is five times lower in stationary – than in exponential phase; (b) cell survival to H2O2 correlates with H2O2 cellular gradients for a variety of cells; and, (c) cells in stationary phase are predicted to be more susceptible to intracellular H2O2 than in exponential phase. In conclusion, limiting H2O2 diffusion into cells is a key protective mechanism against extracellular H2O2.

An integrative mathematical model was developed to obtain an overall picture of lipid hydroperoxide metabolism in the mitochondrial inner membrane and surrounding matrix environment. The model explicitly considers an aqueous and a membrane phase, integrates a wide set of experimental data, and unsupported assumptions were minimized. The following biochemical processes were considered: the classic reactional scheme of lipid peroxidation; antioxidant and pro-oxidant effects of vitamin E; pro-oxidant effects of iron; action of phospholipase A2, glutathione-dependent peroxidases, glutathione reductase and superoxide dismutase; production of superoxide radicals by the mitochondrial respiratory chain; oxidative damage to proteins and DNA. Steady-state fluxes and concentrations as well as half-lives and mean displacements for the main metabolites were calculated. A picture of lipid hydroperoxide physiological metabolism in mitochondria in vivo showing the main pathways is presented. The main results are: (a) perhydroxyl radical is the main initiation agent of lipid peroxidation (with a flux of 10(-7)MS-1); (b) vitamin E efficiently inhibits lipid peroxidation keeping the amplification (kinetic chain length) of lipid peroxidation at low values (approximately equal to 10); (c) only a very minor fraction of lipid hydroperoxides escapes reduction via glutathione-dependent peroxidases; (d) oxidized glutathione is produced mainly from the reduction of hydrogen peroxide and not from the reduction of lipid hydroperoxides.