to produce hydroxyl radicals, whereas Os(IV) oxidizes GSH to GSSG, regenerating Os(III) within cells. This cycle disrupts cellular redox homeostasis, prompting apoptosis and ferroptosis, and displays features of immunogenic cell death. In vivo, both Os(III) and Os(IV) inhibit tumor growth with good tolerability and enhance antitumor immune responses. These findings position redox-cycling metal complexes as a promising strategy to target cancer redox vulnerabilities, encouraging further exploration of combination therapies with immunotherapeutic agents.
Huang et al. (Fri,) studied this question.