Conventional depigmenting agents suppress tyrosinase to reduce melanin but can compromise endogenous photoprotection, resulting in a persistent trade-off between whitening efficacy and UV resilience. Here, we engineer sulfur codoped carbon dots derived from arbutin and niacinamide (N, S-ANCD) to integrate enzymatic inhibition, ROS management, and UVB attenuation within a single ultrasmall nanoplatform. Spectroscopic characterization confirms sulfur incorporation and defect-enriched surface states that broaden UV absorption and favor nonradiative energy dissipation. N, S-ANCD exhibits strengthened tyrosinase inhibition and enhanced DPPH/ABTS radical quenching in vitro while maintaining low cytotoxicity and good hemocompatibility. In zebrafish, N, S-ANCD reduces melanin deposition within a defined safety window and mitigates UVB-induced tail-fin injury in both prevention and posttreatment paradigms. Mechanistically, N, S-ANCD lowers ROS accumulation and lipid peroxidation, restores antioxidant enzyme activities, and reduces injury-associated fluorescence signals consistent with attenuated cell stress. Transcriptomic profiling further indicates coordinated reversal of UV-activated inflammatory and ferroptosis-related programs and normalization of extracellular matrix/adhesion remodeling toward tissue homeostasis. Together, these results demonstrate that sulfur codoped carbon dots enable low-dose depigmentation while maintaining photoprotection, and highlight defect- and surface-state modulation as a viable design principle for multifunctional cosmetic nanomaterials.
Chen et al. (Wed,) studied this question.
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