Fig. 9: Effects of BSO-OxMal and oxaliplatin treatment.
From: A platinum(IV) prodrug strategy to overcome glutathione-based oxaliplatin resistance

Cancer proliferative activity (a) and GSH content (b) as well as DNA damage in tumor (c) and kidney (d) tissues. Mice bearing CT26 allografts (n = 4 per group) were treated twice a week with equimolar concentrations of BSO-OxMal (23.5 mg/kg) or oxaliplatin (9 mg/kg) and sacrificed 24 h after the last drug dosing. Immunohistochemical staining of Ki-67 (a) and the DNA damage parameter pH2AX (c) were quantified in 8–10 regions of interest (ROI) per tumor within random non-necrotic, viable cancer regions by ImageJ software. In (d) cells stained positively for pH2AX in the kidney were counted within 5 ROI per kidney section. Representative images are shown for tumor sections in Supplementary Fig. 14 and for organ sections in Supplementary Fig. 15. In (b) tumor GSH content of the respective cancer samples was quantified by a calorimetric method as described in the methods section. Data in (b, d) are depicted as mean ± SEM (standard error of mean). Statistical significance was tested using one-way ANOVA (a, c) or Student´s t test (b, d). In all cases: *p < 0.05; **p < 0.01; ***p < 0.001.