Comprehensive structural, optical, and biological study of sol–gel-derived Mg₀.₉₁Fe₀.₉O nanoparticles

Non-stoichiometric magnesium–iron oxides are promising multifunctional nanomaterials, yet integrated links between structure, optics, and antimicrobial response remain insufficiently resolved. Here, Mg₀.₉₁Fe₀.₉O nanoparticles were synthesized by a sol–gel route (drying at 100 °C, calcination at 550 °C) and systematically characterized by XRD, FTIR, and UV–Vis, then evaluated biologically against Staphylococcus aureus using the agar diffusion method (ADM) and spread plate method (SPM). FTIR revealed a spinel-type ferrite lattice with characteristic metal–oxygen stretching at ~546 cm⁻¹ (tetrahedral) and ~419 cm⁻¹ (octahedral), alongside surface O–H/H₂O bands at ~3439 and ~1630 cm⁻¹ and a weak carbonate feature near 1468 cm⁻¹, consistent with nanostructured oxides stored in air. The UV–Vis spectrum displayed a sharp ultraviolet edge and a weak sub-gap tail. Tauc analysis of (αhν)2 versus hν (direct-allowed transition) yielded an optical band gap Eg=3.85 eV, indicating an electronically wide-gap oxide in which visible-light activity is expected to be dominated by defect/surface states rather than bulk interband absorption. Antibacterial testing against S. aureus showed a clear inhibition halo in ADM with diameter D=16 mm (ring width ≈ 5 mm; net inhibitory area Anet≈172.8 mm² for a 6-mm disc), indicating moderate potency at the tested loading. Complementary SPM quantified surviving cells at 275 colony-forming units (CFU), within the 30–300 countable range (Poisson relative standard error ≈ 6%), confirming a finite but reduced viable fraction after exposure. Collectively, the results connect phase-consistent structure and a wide optical gap to reproducible anti-staphylococcal activity, plausibly mediated by reactive oxygen species and limited ion release. Future work should include matched controls for log-reduction metrics, increased replication, dispersion standardization, and contact/light-assisted assays to resolve defect-driven pathways.