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Abstract Ascorbate (H 2 A) is a well‐known antioxidant to protect cellular components from free radical damage and has also emerged as a pro‐oxidant in cancer therapies. However, such “contradictory” mechanisms underlying H 2 A oxidation are not well understood. Herein, we report Fe leaching during catalytic H 2 A oxidation using an Fe−N−C nanozyme as a ferritin mimic and its influence on the selectivity of the oxygen reduction reaction (ORR). Owing to the heterogeneity, the Fe‐N x sites in Fe−N−C primarily catalyzed H 2 A oxidation and 4 e − ORR via an iron‐oxo intermediate. Nonetheless, trace O 2 ⋅ − produced by marginal N−C sites through 2 e − ORR accumulated and attacked Fe‐N x sites, leading to the linear leakage of unstable Fe ions up to 420 ppb when the H 2 A concentration increased to 2 mM. As a result, a substantial fraction (ca. 40 %) of the N−C sites on Fe−N−C were activated, and a new 2+2 e − ORR path was finally enabled, along with Fenton‐type H 2 A oxidation. Consequently, after Fe ions diffused into the bulk solution, the ORR at the N−C sites stopped at H 2 O 2 production, which was the origin of the pro‐oxidant effect of H 2 A.
Cao et al. (Fri,) studied this question.