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The anti-tumor effect of therapeutic carbon monoxide (CO) has been considered concerning the electron transport chain on the inner mitochondrial membrane. Herein, a tumor microenvironment and photo-responsive CO nanoplatform Ca-Flav nanoparticles (NPs) were constructed through biomineralizing acryloyl-modified flavonol, which could release CO both in normoxia and hypoxia conditions upon irradiation at tumor lesion. The in vitro experiments demonstrated that the endoplasmic reticulum stress-related signal pathways could be activated through oxidative stress caused by CO mediated mitochondrial biogenesis and calcium ion turbulence induced by Ca3(PO4)2 acidolysis, resulting in mitochondrial dysfunction and cell apoptosis. In addition, the Ca-Flav NPs exhibited excellent biocompatibility and tumor inhibition effect in vivo. This work provides new insight into the potential characteristics of CO, paving a new way to engineer more efficient treatment based on CO.
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