Mechanism of Antibacterial Activity of Nanomaterials

Nanomaterials exhibit antibacterial potentials manifested as disintegration of the cell membrane leading to leakage of the cytoplasmic contents followed by the lysis of the bacterial cells [47,76,77]. Passive internalization of the NPs can occur through porin-ion channels in Gram-negative bacteria [78], whereas in Gram-positive bacteria, presence of thick cell wall hinders passive internalization and therefore, dissolved ionic species (e.g., Zn2+, Cu2+, and Fe2<sup>+</sup> ions) released by the nanoparticles in vicinity of the cell surface get chelated by lipoteichoic acid [79]. Once inside the cell, the internalized NPs may elicit Fenton- or non-Fenton-based ROS-mediated damage of the plasma membrane, internal macromolecules, and other soluble and catalytic biomolecules [78]. Eventually or simultaneous release of ions by the dissolution of NPs leads to metal/nonmetal ion toxicity culminating to cell death [25,76]. Another interesting mechanism involves inhibited expression of the quorum-sensing regulated genes or functions in bacteria leading to inhibition of the biofilm formation [41,80]. The nanostructured materials can also help in the inhibition of the preformed biofilms of the plant pathogens, which is of great significance for the eradication of resistant bacterial pathogens [81] or pathogens related to food spoilage [80,82].
