Abstract The green synthesis approach has drawn a lot of interest as an environmentally friendly and sustainable acceptable means of producing a diverse range of nanoparticles (NPs). This piece described a rapid approach for synthesizing selenium nanoparticles (SeNPs) with grape seed extract. A biologically active composition of selenium-chitosan nanoparticles (Se-chitosan NPs) has been prepared and characterized using, ultraviolet–visible, scanning electron microscopy, transmission electron microscopy, and zeta potential and size distribution experiments. To study the anticancer activity of prepared NP cytotoxicity (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay of chitosan nanoparticles (Chito-NPs), SeNPs were tested on two cancer cell lines: A549 and normal cell line (HK-2). In addition to a series of morphological changes, induction of apoptosis, reactive oxygen species (ROS) generation, and mitochondrial membrane potential. The results showed that the synthesized NPs were spherical with 55.285 and 30.9 nm, for SeNPs and Se-chitosan NPs, respectively. In the A549 cell line, SeNPs and Se-chitosan NPs exhibited dose-dependent cytotoxicity, with an IC50 for Chito-NPs of 24.09 µg/mL, whereas for SeNPs it was 18.56 µg/mL. Conversely, normal cell lines (MCF-10) were not significantly cytotoxically affected by SeNPs and Se-chitosan NPs. Additionally, SeNP and Se-chitosan NP treatment resulted in increased ROS generation and caused mitochondrial dysfunction. Based on ROS-mediated pathways, the results demonstrated that Chito-NPs, SeNPs, and Se-chitosan NPs cause apoptosis and death in A549 cells. As nanotherapeutics, Chito-NPs, SeNPs, and Se-chitosan NPs appear to offer a great deal of unrealized potential based on these findings. Further investigation is warranted and clinically significant to elucidate the specific therapeutic potential and safety of these NPs when applied in vivo. In this work, we show that exposure to SeNPs, Chito-NPs, and Se-chitosan NPs alters the human lung cancer cell line A549’s ROS route of signaling, thereby causing the induction of apoptosis.
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