(A-C) Mitochondria are the source of cisplatin-induced ROS in cancer cells.

<p>Representative flow cytometry curves of total intracellular ROS levels (H₂DCFDA) in (<b>A</b>) DU145 and (<b>B</b>) isogenic DU145ρ^° cells following 24 h of exposure to cisplatin at an IC50 dose (20 μM). H₂O₂ was used as positive control. (<b>C</b>) Quantitative representation of previous experiment. Data are presented as fold increase over no treatment. Bars represent the mean of n=3 independent biological replicates +/- SD. ROS levels in treated vs. non treated cells in DU145 and DU145ρ^° genotypes were analyzed by two-way ANOVA (treatment x genotype interaction p<0.05; Bonferroni post-test for multiple comparison: ** p<0.01). (<b>D</b>-<b>F</b>) <b>Mitochondrial ROS contribute to the cell killing effect of cisplatin</b>. (<b>D</b>) Survival of DU145 and isogenic DU145ρ^° after exposure to a dose range of cisplatin. (<b>E</b>) DU145 and (<b>F</b>) DU145ρ^° cell survival after exposure to a dose range of cisplatin with or without 1 mM of NAC. Data represent mean of n=3 independent experiments +/- SD. **p<0.005, ***p<0.0005.