Proposed mechanism of QD induced cell death involving Fas, lipid peroxidation and mitochondrial impairment. Cells exposed to cadmium telluride quantum dots (unmodified and NAC-modified) induce ROS which causes Fas upregulation and plasma membrane lipid peroxidation. Apoptotic cell death is induced by activation of Fas and its downstream effectors. Lipid peroxidation also occurs at the mitochondrial membranes, degrading cardiolipin, changing the mitochondrial membrane potential, eventually leading to the release of cytochrome c , and promoting apoptotic cascades. NAC bound to the QD surface, modifies the extent of QD internalization, which is correlated with cell death, upregulation of Fas, and ROS induced lipid peroxidation. NAC treatment (2–5 mM) abolishes oxidative stress, induces antioxidant enzymes and attenuates mitochondrial impairment.