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Anthracyclines are used in the treatment of childhood cancer and contribute to survival rates exceeding 80%. Despite this, anthracycline-induced cardiotoxicity is a major long-term complication in survivors. The mechanisms underlying this toxicity are complex, though elevations in intracellular oxidative stress are thought to play a role. However, this has not been measured directly, and the sources of reactive oxygen species remain unclear. To begin to elucidate this formed the aim of our study. Cardiac myoblasts (H9c2) were loaded with CM-DCFDA for photometric measurement of intracellular oxidative stress. Doxorubicin, daunorubicin, idarubicin and epirubicin increased intracellular oxidative stress by 76.5 ± 4.9 % (n = 31, p < 0.0001), 62 ± 4.1 % (n = 20, p < 0.0001), 47.1 ± 2.5 % (n = 20, p < 0.0001) and 44.2 ± 6.1 % (n = 23, p < 0.0001) respectively. In most cases, this was attenuated by preincubation with the antioxidant N-Acetyl Cysteine, NADPH oxidase (NOX) inhibitor; VAS2870 and Xanthine Oxidoreductase (XOR) inhibitor; febuxostat. These preliminary findings suggest that anthracyclines can elevate cardiac intracellular oxidative stress, and this is partially NOX and XOR dependent. Future experiments will further elucidate the sources of oxidative stress, and association with dysregulated calcium signalling.