Figure 9.

NMs-induced various cellular responses in KCs. This includes the metal or metal oxide (MOx) or transition-metal oxide (TMO) NMs, e.g., Ag, CuO, Co₃O₄, or Mn₂O₃, induce apoptosis due to their dissolution and shedding of toxic ions, bandgap energy, and oxidative stress; REOs (e.g., Gd₂O₃, La₂O₃, and Y₂O₃) and GOs induced pyroptosis in KCs. For REOs, the transformation from sphere to sea urchin-shaped and the formation of rare-earth phosphate (REPO₄) structures on the lysosomal membrane, where RE(III) ions strip phosphate from the phospholipids on a lysosomal membrane and induce lysosomal damage, cathepsin B release, leading to NLRP3 inflammasome activation and GSDMD-mediated pyroptosis; the phagocytized GOs-induced NADPH oxidase activation and lipid peroxidation, triggering PLC activation that leads to calcium flux, mitochondrial ROS generation, and NLRP3 inflammasome activation, resulting in IL-1β production as well as subsequent pyroptosis; for fumed SiO₂, the activation of NLRP3 inflammasome is involved in the pathway premised on K⁺ efflux resulting from the plasma membrane perturbation after SiO₂ binding. Moreover, 2D TMD, CNCs, and CNTs induce ROS-mediated apoptosis and inflammatory responses in KCs after their internalization.