Silver nanoparticles biofabricated from the Red Alga Acanthophora spicifera: Green synthesis, physicochemical characterization, multifaceted bioactivity, and toxicity assessment
Abstract
Anti-microbial resistance (AMR) pathogens increasingly rely on biofilm formation as a primary survival mechanism, necessitating the development of novel antimicrobial agents. In this study, biogenic silver nanoparticles (As-AgNPs) were synthesized using a green synthesis, facilitated by the aqueous extract of the marine macro-algae Acanthopora spicifera. UV-Visible spectroscopy confirmed nanoparticle formation with a characteristic surface plasmon resonance (SPR) peak at 420 nm. Structural analysis via X-ray diffraction (XRD) confirmed a face-centered cubic (fcc) crystalline lattice with a primary crystallite size of 36.08 nm, while Scanning Electron Microscope (SEM) micrographs revealed spherical morphology with a mean physical diameter of 45.78 nm. In contrast, Dynamic Light Scattering (DLS) analysis showed a significantly larger hydrodynamic diameter of 277.2 nm, attributed to the robust bio-organic capping layer from the algae, which also imparted high colloidal stability with -59.1 mV Zeta potential. Functional assays demonstrated that As-AgNPs possess superior anti-oxidant efficacy, achieving 86.0 ± 1.0 % free radical scavenging compared to the raw extract (72.3 ± 2.5 %). Antibacterial screening showed potent inhibition against Escherichia coli, Acinetobacter baumanii and Enterococcus faecalis (MIC: 31.25 µg/Ml), with Staphylococcus aureus exhibiting a threshold of 62.5 µg/mL. Anti-biofilm assay activity against a high biofilm producing clinical isolate of Pseudomonas aeruginosa revealed 66 ± 8.544 % inhibition with a calculated IC50 of 211.58 µg/mL. Toxicity assessments in Danio rerio embryos established a concentration dependent safety profile (5-10 mg/L), with a hatching EC50 of 67.01 mg/L. These findings suggest that A. spicifera mediated silver nanoparticles are highly stable, biocompatible and may serve as potent agents for disrupting the biofilm architecture of MDR clinical pathogens.