β-cypermethrin (BCP) is a broad-spectrum insecticide known for its rapid efficacy. However, it is highly toxic to non-target organisms such as bees and fish, and its effectiveness is limited by a short duration of action. Improving the release profile of BCP is essential for reducing its environmental toxicity while preserving its effectiveness. In this study, hollow mesoporous silica nanoparticles (HMSNs) were synthesized using a self-templating method, and BCP-loaded HMSNs were prepared through physical adsorption. The structural and physicochemical properties of the nanoparticles were characterized using scanning electron microscopy (SEM), transmission electron microscopy (TEM), nitrogen adsorption–desorption analysis, Fourier transform infrared (FT-IR) spectroscopy, dynamic light scattering (DLS), and thermogravimetric analysis (TGA). The BCP release profile was assessed using the dialysis bag method. The results showed that the synthesized nanoparticles exhibited uniform morphology, thin shells, and large internal cavities. The HMSNs had a pore size of 3.09 nm, a specific surface area of 1318 m²·g⁻¹, a pore volume of 1.52 cm³·g⁻¹, and an average particle size of 183 nm. TEM, FT-IR, and TGA analyses confirmed the successful incorporation of BCP into the HMSNs, achieving a drug loading efficiency of 32.53%. The BCP-loaded nanoparticles exhibited sustained-release properties, with an initial burst followed by gradual release, extending efficacy for 30 days. Safety evaluations revealed minimal toxicity to maize seedlings, confirming the biocompatibility of the nanoparticles. These findings indicate that BCP-loaded HMSNs can enhance the efficacy of BCP while reducing its environmental toxicity, providing a biocompatible and environmentally friendly solution for pest control.

Schisandra is a plant whose fruit possesses high biological potential and beneficial health effects. The pharmacological properties of Schisandra are attributed to its bioactive components, primarily polyphenols and polysaccharides. This study aimed to obtain Schisandra fruit extracts (SCE) from different locations in China and Poland, as well as Schisandra polysaccharides (SPO), and to compare their chemical composition and selected biological activities. The prebiotic and antibacterial effects of SCE and SPO on lactic acid bacteria (LAB), human and foodborne pathogens, and gut microbiota were investigated. The chemical composition of the three Chinese SCE was similar, whereas SCE from Poland (SCE-PL) differed. The main bioactive compounds differentiating the Chinese SCE were quercetin, isorhamnetin, and nicotiflorin, while gamma-tocopherol and mevalonic acid distinguished SCE-PL, as indicated through LC-QTOF-MS/MS metabolomic profiling. All SCE and SPO promoted the growth of LAB strains, confirming their prebiotic potential and ability to serve as effective carbon sources for LAB. Additionally, all SCE inhibited the growth of certain pathogens, with S. chinensis extract from China showing the strongest activity, whereas SPO did not exhibit such activity. Variations in chemical composition among SCE and SPO contribute to differences in their prebiotic and antimicrobial activity, highlighting the importance of species and geographical origin in determining their functional properties.

Conjugated linolenic acids (CLnAs) are emerging as promising agents to trigger ferroptosis, a cell death driven by excessive lipid peroxidation, in cancer cells. Given the aggressive nature and treatment resistance of malignant melanoma, exploring CLnAs as therapeutic agents may offer a novel strategy to overcome these challenges. Here, we investigated the toxicity of four CLnA isomers on human (A375, WM266.4) and zebrafish (ZMEL1) melanoma cell lines. We observed a dose-dependent reduction in cell viability across all three tested cell lines. While human melanoma cells were more sensitive to CLnAs than ZMEL1 cells, treatment with ferroptosis inhibitors mitigated cell death in all models, confirming ferroptosis as the consistent primary mechanism of cell death. In addition, chemical inhibitors of ACSL4 and GPX4 modulated CLnA toxicity, further substantiating the ferroptotic mechanism by highlighting the role of these key regulators. Furthermore, fatty acid analysis revealed that CLnAs were effectively incorporated into phospholipids, generating substrates for lethal lipid peroxidation. At the transcriptional level, CLnA treatment significantly upregulated the pro-ferroptotic gene acsl4a in ZMEL1 cells. Overall, our study identifies specific CLnAs as potent ferroptosis inducers in both human and zebrafish melanoma cells and underscores the translational relevance of the zebrafish model based on a shared ferroptotic mechanism.

Conjugated linolenic acids (CLnAs) are emerging as promising agents to trigger ferroptosis, a cell death driven by excessive lipid peroxidation, in cancer cells. Given the aggressive nature and treatment resistance of malignant melanoma, exploring CLnAs as therapeutic agents may offer a novel strategy to overcome these challenges. Here, we investigated the toxicity of four CLnA isomers on human (A375, WM266.4) and zebrafish (ZMEL1) melanoma cell lines. We observed a dose-dependent reduction in cell viability across all three tested cell lines. While human melanoma cells were more sensitive to CLnAs than ZMEL1 cells, treatment with ferroptosis inhibitors mitigated cell death in all models, confirming ferroptosis as the consistent primary mechanism of cell death. In addition, chemical inhibitors of ACSL4 and GPX4 modulated CLnA toxicity, further substantiating the ferroptotic mechanism by highlighting the role of these key regulators. Furthermore, fatty acid analysis revealed that CLnAs were effectively incorporated into phospholipids, generating substrates for lethal lipid peroxidation. At the transcriptional level, CLnA treatment significantly upregulated the pro-ferroptotic gene acsl4a in ZMEL1 cells. Overall, our study identifies specific CLnAs as potent ferroptosis inducers in both human and zebrafish melanoma cells and underscores the translational relevance of the zebrafish model based on a shared ferroptotic mechanism.