In this study, electrically conductive polymer composites based on repellent N,N-diethyl-3-methylbenzamide with concentrations ranging from 6 to 30 wt% were developed. The electrical resistivity of repellent composites, as determined by electrochemical impedance spectra, ranges from 150 to 171 Ohm, which allows such materials to be used when a low voltage is applied. The study of the rheological properties of the obtained repellent composites and the analysis of the TGA curves demonstrated that the dynamic viscosity of the materials has a significant effect on the thermal diffusion of the repellent. The study of the thermal diffusion of N,N-diethyl-3-methylbenzamide demonstrated that a higher yield of repellent (up to 36.4 × 10⁻⁸ mol) is achieved when the material is applied in the form with the shortest conductor length of 14 mm. The graphs showing the relationship between the electrical flux and the concentration of N,N-diethyl-3-methylbenzamide, which was calculated via the Peltier and Thompson equations, show that, according to Onsager’s theory, the total flux of the substance is highest when a voltage is applied to the material with the shortest conductor length. Thus, the developed repellent composite is a promising material for protection against blood-sucking insects.

Hydrogen sulfide (H₂S) is a vital gasotransmitter essential for maintaining redox homeostasis and modulating inflammatory responses. Herein, we examined a collection of Drosophila melanogaster knockout (KO) lines generated in our laboratory, lacking key genes involved in transsulfuration (cbs, cse) and sulfide metabolism (tst1), to elucidate the role of this adaptive system in immunity. Genetic ablation of these pathways results in profound H₂S deficiency and hyperhomocysteinemia, leading to chronic oxidative stress. This leads to constitutive activation of major immune pathways—including IMD, Toll, and JAK-STAT—even in the absence of infection, a hallmark of chronic inflammation. Indeed, transcriptomic analysis and qRT-PCR studies revealed significant upregulation of these pathways in double (cbs; cse) and triple (cbs; cse; tst1) KO flies under control conditions. Following septic injury with Bacillus subtilis, double and triple KO flies exhibited increased expression of antimicrobial peptides (AMPs) and pattern recognition receptors compared to control and TST1-/- single KO lines. Notably, double and triple KO lines showed more prolonged immune activation. The triple KO flies exhibited the worst survival rate following septic injury. These results demonstrate that H₂S deficiency causes chronic inflammation through the sustained activation of immune pathways, highlighting sulfur metabolism as a crucial regulator of homeostasis and innate immunity in Drosophila.

Hydrogen sulfide (H₂S) is a vital gasotransmitter essential for maintaining redox homeostasis and modulating inflammatory responses. Herein, we examined a collection of Drosophila melanogaster knockout (KO) lines lacking key transsulfuration (cbs, cse) and sulfide metabolism (tst1) genes, generated in our laboratory, to elucidate the role of this adaptive system in immunity. Genetic ablation of these pathways results in profound H₂S deficiency and hyperhomocysteinemia, leading to chronic oxidative stress. This leads to constitutive activation of major immune pathways—including IMD, Toll, and JAK-STAT—even in the absence of infection, a hallmark of chronic inflammation. Indeed, transcriptomic analysis and qRT-PCR studies revealed significant upregulation of these pathways in double (cbs;cse) and triple (cbs;cse;tst1) KO flies under control conditions. Following septic injury with Bacillus subtilis, double and triple KO flies exhibited increased expression of antimicrobial peptides (AMPs) and pattern recognition receptors compared to control and TST1-/- single KO lines. Notably, double- and triple-KO lines showed more prolonged immune activation. The triple KO flies exhibited the worst survival rate following septic injury. These results demonstrate that H₂S deficiency causes chronic inflammation through the sustained activation of the immune pathways, highlighting sulfur metabolism as a crucial regulator of homeostasis and innate immunity in Drosophila.