Magnesium oxide nanoparticles (MgONPs) demonstrate size-influenced antibacterial activity against Ralstonia solanacearum, with physical disruption mechanisms appearing to play a more prominent role than reactive oxygen species (ROS) effects under the tested conditions. While 30 nm particles generated maximum ROS levels, 20 nm MgONPs exhibited superior bactericidal efficacy, reducing survival to 36% at 300 mg/L versus 46% for 30 nm particles-a superiority consistently supported by motility, membrane, and transcriptomic assessments even at the complete-killing concentration (500 mg/L). This size-dependent efficacy was further validated in vivo. ROS scavenging tests and transcriptomics suggested that oxidative stress may not be the primary driver of antimicrobial action, though a potential synergistic role cannot be entirely excluded. The primary mechanisms involved size-specific physical membrane damage, DNA integrity changes, and metabolic interference. Smaller particles (20 nm) caused significant membrane destabilization and uniquely disrupted acetyl-CoA metabolism and oxidoreductase activity through downregulation of ribosome biogenesis, oxidative phosphorylation, and amino acid degradation pathways. Transcriptomic profiling revealed that particle size modulates catabolic gene expression and redox-related processes, with 20 nm particles inducing distinct metabolic suppression patterns. This study provides insights into the ongoing debate regarding ROS versus physical mechanisms, suggesting that nanoscale precision combined with surface properties governs antibacterial efficiency. The findings position MgONPs as a tunable antimicrobial platform where optimized particle dimensions and formulation strategies enhance pathogen control through targeted physical disruption and metabolic interference. These mechanistic insights offer a basis for engineering nanomaterials with improved bactericidal performance via optimization of multiple physicochemical properties.
Nie et al. (Sun,) studied this question.