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. 2023 May 9;15(6):e16910. doi: 10.15252/emmm.202216910

Figure 4. Ascorbate potentiates IACS‐010759‐induced cell death by increasing oxidative stress.

Figure 4

  1. Viability of FLMycER and BaFMycER cells primed or not with 100 nM OHT and treated with 135 nM IACS‐010759 for 48 h and/or with ascorbate at the indicated concentration for 6 h. n = 3 biological replicates; error bars: SD.
  2. 405/488 nm fluorescence ratio from the cytoplasmic Grx1‐roGFP2 reporter in FLMycER cells treated with 400 μM ascorbate (Asc) for the indicated periods of time, either with IACS‐010759 (36 h, left) or without it (right). The same experiment with OHT‐primed cells is shown in Appendix Fig S4D.
  3. Cell viability of FL5.12 cells at the end of treatment (48 h IACS‐010759, 6 h Asc), in the presence or absence of 50 μM deferoxamine (DFX, added 1 h before Asc). n = 3 biological replicates; error bars: SD.
  4. Quantification of lipid peroxides in FL5.12 cells treated with 135 nM IACS‐010759 for 24 h and/or 400 μM Asc for 3 h. **P ≤ 0.01; *P ≤ 0.05 (one‐way ANOVA). Each point in the graph is from an independent biological replicate and represents the average of thousands of events (single cells) in a distinct cell population, normalized to the untreated condition. Single‐cell measurement distributions from a representative experiment are provided in Appendix Fig S4F.

Source data are available online for this figure.