Visualizing GSH-ONOO− Redox and Tracking Lesion-Remedy of Acute Kidney Oxidative Injury Based on a Dual-Site Chemosensor

Drug-induced acute kidney injury (DIAKI) is strongly associated with the accumulation of peroxynitrite (ONOO − ) and the depletion of glutathione (GSH), both of which contribute to increased morbidity and mortality. Owing to the lack of an effective method for the real-time monitoring of nephrotoxicity, it remains a diagnostic and therapeutic challenge and is considered a significant issue in clinical practice. Herein, a dual-site fluorescent chemosensor, BPS is developed , which enables the simultaneous real-time monitoring of ONOO − and GSH through distinct channels (ONOO − : λ ex = 410 nm, λ em = 548 nm; GSH: λ ex = 490 nm, λ em = 660 nm) without spectral crosstalk. The sensor displays remarkable sensitivity toward ONOO − and GSH, with low detection limits (181 n m and 2.42 µ m , respectively), exceptional specificity, and anti-interference effects. BPS is used to monitor ONOO − /GSH in real time to track the lesion of cisplatin-stimulated DIAKI and the following remedy process in mice and HK-2 cells for the first time. BPS provides a feasible tool for investigating oxidative stress-related DIAKI disease processes and further exploring some physiological mechanisms. Moreover, this study also offers a strategy for visualizing, modulating, and controlling the intracellular GSH/ONOO − redox.