Antioxidants prevent BCR/ABL-induced ROS-mediated mutations in BCR/ABL kinase domain and mouse α1 subunit of Na⁺/K⁺ ATPase in vitro. 32Dcl3 parental (P-early) and 2-week-old 32Dcl3-p210BCR/ABL cells (B/A-early, no mutations detected in BCR/ABL kinase and mouse α1 Na⁺/K⁺ ATPase) were cultured for 8 weeks in medium supplemented with IL-3 (B/A) and IM (B/A + IM), PDTC (B/A + PDTC), or IM and BSO (B/A + IM + BSO). The percentage of IM-resistant cells (A, % of IM-resistant cells) and ouabain-resistant cells (B, % of ouabain-resistant cells) was determined by clonogenic assay performed in the absence of IL-3 and the presence or absence of IM or ouabain, respectively. Mutation rate and mutation phenotype in BCR/ABL kinase and mouse α1 subunit of Na⁺/K⁺ ATPase are shown in panels A and B, respectively. Mutations leading to previously described amino acid substitutions are listed (Aa substitutions in panels A and B, respectively). ^*P < .05 compared with B/A group; ^**P < .05 compared with other groups.