Fig. 4: ROS storm cascade generation and amplification of oxidative stress.
a Schematic diagram of O2•- mediated Type I PDT mechanism. b, c Detection of O2•- of SMNB+hv, SNH2C4+hv, SNH2C4H+hv and dihydrorhodamine 123 (DHR123) in normoxia (N) and hypoxia (H) (n = 3 independent experiments; mean values  ±  SD). d ROS detection in B16 and MCF-7 cells using DCFH-DA, DHR123, and hydroxyphenyl fluorescein (HPF) as total ROS, O2•-, and •OH fluorescence indicator, respectively (Blue: DAPI, Green: DCFH-DA/HPF ROS tracker; Red: DHR123 ROS tracker). Three independent experiments were performed and representative results are shown. Scale bar = 40 μm. e The CLSM images of mitochondrial membrane potential (MMP) in B16 and MCF-7 cells subjected to different treatments assessed by JC-10 assays (Green: J-monomer; Red: J-aggregates). Three independent experiments were performed and representative results are shown. Scale bar = 40 μm. f Schematic illustration of sequential oxidative impairment of biomacromolecules. g Lipid peroxidation products (Malondialdehyde, MDA) detection (n = 4 independent experiments; mean values  ±  SD). h The level of 8-hydroxy-2-deoxyguanosine (8-OHdG) was measured by Elisa kit assay after different treatments (n = 4 independent experiments; mean values  ±  SD). i Intracellular glutathione in B16 and MCF-7 cells treated with SHC4+hv, SHC4H, SHC4H+hv. Reduced glutathione (GSH)/oxidized glutathione (GSSG) was reported as the ratio of GSH to GSSG (n = 6 independent experiments; mean values  ±  SD). Statistical differences were determined by One-way ANOVA with a Tukey post-hoc test. Source data are provided as a Source Data file.
