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. 2019 May 23;11(5):712. doi: 10.3390/cancers11050712

Figure 4.

Figure 4

Hu.A induced mitochondrial reactive oxygen species (ROS) production and mitochondrial damage in DLD-1 cells. DLD-1 cells were treated with Hu.A for indicated time points in serum-free condition. The cells were stained with MitoSOX™ (Thermo Fisher Scientific, Rockford, IL, USA) Red (A and B), and tetramethylrhodamine methyl ester (TMRM) (C and D). The fluorescence for both assays was measured by FACS analysis. The relative mitochondrial ROS and TMRM fluorescence levels were calculated to determine the fold difference in comparison to control and are shown as mean ± SD. ***, p < 0.001. (E) In the serum-free condition, the cells were pre-treated with MitoTEMPO (Sigma-Aldrich, St. Louis, MO, USA) (50 μM) for 1 h and treated with 3 μM of Hu.A for 6 h. MTT assay was then performed. Data are indicated as mean ± SD. ***, p < 0.001 compared with the only Hu.A-treated group and MitoTEMPO with Hu.A co-treated group.