Hypochlorous acid (HClO) has been gradually recognized as a significant reactive oxygen species (ROS) owing to its stability in organisms. ROS concentration in cancerous cells is approximately ten times that in normal cells and excessive HClO is closely associated with tissue damage. Herein, a new turn-on fluorescent probe (MOBT-Cl) based on ESIPT for sensing HClO has been synthesized. MOBT-Cl possessed a large Stokes shift (130 nm), a rapid response time (around 10 s), and ultra-sensitivity (110-folds, LOD = 0.14 nM). Moreover, MOBT-Cl was suc-cessfully applied to imaging HClO in cells, zebrafish, and mice. Importantly, MOBT-Cl effectively distinguished cancerous cells from normal cells and monitored HClO levels in APAP-treated cells and zebrafish as well as diagnosed APAP-induced liver injury. The proposed probe held great potential for investigating the precise role of HClO in multiple physiological processes.

As a reliable signaling biomolecule for oxidative stress, the accurate hypochlorous acid (HClO) detection during agent-stimulated oxidative stress plays a vital role in pathological and physiological mechanism exploration for disease theranostics. Therefore, the development of robust analytical tools for HClO is highly significant. Herein we presented an ESIPT fluorescent probe (MEBTA-Cl) for HClO detection. MEBTA-Cl exhibited ultrarapid-response (around 6 s), high sensitivity (42-folds) and low detection limit (7.8 nM) toward HClO titration in solution. MEBTA-Cl was capable to detect both exo-/endogenous HClO in living cells. Moreover, MEBTA-Cl was successfully employed to monitor HClO level in acetaminophen (APAP), disulfiram (DSF) and doxorubicin (DOX)-stimulated oxidative stress. Importantly, using this useful probe, it was available to detect HClO in li-popolysaccharides (LPS) and APAP treated zebrafish.

Hydrogen peroxide (H2O2) is closely related to a variety of human diseases. It is a challenge to dynamically monitor biological H2O2 activity. Hence, we design and prepare a NIR-emitting ratiometric fluorescent probe (HBQ-B) for detecting H2O2 according to the excited-state intramolecular proton transfer (ESIPT) mechanism using the benzyl bomnic pinacol ester group as a recognition unit. HBQ-B displayed specificity toward H2O2 over other bioactive analytes. Meanwhile, HBQ-B exhibited a good linear relationship between the fluorescence ratio (I-656/I-530) changes and the concentrations of H2O2 (0-10 mu M). HBQ-B also showed a large Stokes shift (234 nm) and a marked detection limit (40.2 nM). HBQ-B was utilized to image the intracellular H2O2 in living MCF-7 cells, HeLa cells and macrophages (RAW 264.7 cells), respectively. In addition, HBQ-B was used to monitor the dynamics of H2O2 level changes during zebrafish development.

Photodynamic therapy (PDT) is a promising cancer therapy modality due to its intrinsically negligible side effects and treatment resistance. However, the development of the high-efficiency PDT still remains a challenge. Herein, a nanodrug platform PEG-Ce6-PEI@PB combined tumor acidity-induced polyethyleneimine (PEI) cytotoxicity with an oxygen self-supply property is developed for dual-enhanced PDT. The obtained PEG-Ce6-PEI@PB presents suppressed PEI cytotoxicity and chlorin e6 (Ce6) phototoxicity during the bloodstream before becoming active in tumor tissues/cells. The acidic tumor microenvironment can shed PEG coating to rebound PEI positive charges, facilitating tumor cell uptake and reverting the PEI cytotoxicity to enhance following PDT. Moreover, Prussian blue (PB) nanozymes with catalase-like activity can convert endogenous hydrogen peroxide into oxygen to relieve tumor hypoxia, which is attributed to the photosensitizer Ce6 producing more cytotoxic reactive oxygen species upon laser irradiation to further strengthen PDT. Moreover, PEG-Ce6-PEI@PB exhibits good biocompatibility and long blood circulation. More importantly, PEG-Ce6-PEI@PB-treated breast cancer cells and tumor-bearing mice present effective therapeutic efficacy upon laser irradiation, verifying the synergistic antitumor effects of PEI cytotoxicity and oxygen self-supplying PDT.