An Organic–Inorganic Hybrid Nanocomposite as a Potential New Biological Agent

• Main Authors: Mateusz Dulski, Katarzyna Malarz, Michał Kuczak, Karolina Dudek, Krzysztof Matus, Sławomir Sułowicz, Anna Mrozek-Wilczkiewicz, Anna Nowak
• Format: Article
• Language: English
• Published: MDPI AG 2020-12-01
• Series: Nanomaterials
• Subjects: chemical reduction; silver-silica nanocomposite; carboxymethylcellulose; sodium alginate; physicochemical features; antimicrobial activity
• Online Access: https://www.mdpi.com/2079-4991/10/12/2551

To solve the problem of human diseases caused by a combination of genetic and environmental factors or by microorganisms, intense research to find completely new materials is required. One of the promising systems in this area is the silver-silica nanocomposites and their derivatives. Hence, silver and silver oxide nanoparticles that were homogeneously distributed within a silica carrier were fabricated. Their average size was d = (7.8 ± 0.3) nm. The organic polymers (carboxymethylcellulose (CMC) and sodium alginate (AS)) were added to improve the biological features of the nanocomposite. The first system was prepared as a silver chlorine salt combination that was immersed on a silica carrier with coagulated particles whose size was d = (44.1 ± 2.3) nm, which coexisted with metallic silver. The second system obtained was synergistically interacted metallic and oxidized silver nanoparticles that were distributed on a structurally defective silica network. Their average size was d = (6.6 ± 0.7) nm. Physicochemical and biological experiments showed that the tiny silver nanoparticles in Ag/SiO₂ and Ag/SiO₂@AS inhibited <em>E. coli</em>, <em>P. aeruginosa</em>, <em>S. aureus</em>, and <em>L. </em><em>plantarum's</em> cell growth as well as caused a high anticancer effect. On the other hand, the massive silver nanoparticles of Ag/SiO₂@CMC had a weaker antimicrobial effect, although they highly interacted against PANC-1. They also generated reactive oxygen species (ROS) as well as the induction of apoptosis via the p53-independent mechanism.