Schematic mechanism of CaO2@HMSNs-PAA serving as tumor environment-responsive nanoparticles for the antitumor therapy of prostate cancer. The natural pH value of the blood and normal tissues can prevent the release of H2O2 from CaO2@HMSNs-PAA. However, the acidic tumor environment (TME) contributes to the responsive release of CaO2, followed by the tendency to generate more H2O2. In addition, after intracellular uptake of CaO2@HMSNs-PAA by endocytosis, the more acidic environment in the lysosomes can result in the enhanced release of H2O2. Compared with normal cells, the extra exogenous ROS that has accumulated in tumor cells cannot be effectively decomposed because of the elevated basal level of ROS and the overburdened antioxidant system, consequently inducing the mitochondria-mediated apoptosis via remarkable oxidative stress.