Oxidative stress (OS) is caused by excessive production of reactive oxygen species (ROS) and/or impaired antioxidant defence mechanisms. In oocytes, exposure to high ROS is associated with defective embryo development, apoptosis and embryonic arrest. The aims of current study were to determine 1) the mechanisms by which OS in cumulus-oocyte complexes (COCs) impairs subsequent embryo development and 2) the ability of the drug BGP-15, a ROS inhibitor, to alleviate any cellular defects. To induce OS, mouse ovulated COCs were treated acutely with hydrogen peroxide (H2O2; 50mM for 30 minutes), followed by in-vitro fertilisation (IVF) and embryo development assessments. These included differential staining to examine allocation of cell numbers, CM-H2DCFDA to measure intracellular ROS levels, JC-1 to assess mitochondrial membrane potential (MMP) and quantification of mitochondrial DNA (mtDNA) copy number to assess replication. Exposure of COCs to H2O2 significantly impaired cleavage rate following IVF (p<0.05) but not subsequent blastocyst formation. BGP-15 treatment improved blastocyst development (p<0.05) particularly in embryos from H2O2-treated COCs. Differentiation was altered as shown by a reduction in cell numbers in the embryos generated from the H2O2-treated COCs; and this was normalised with BGP-15 treatment. ROS levels in embryos from H2O2-exposed oocytes were not different compared to control embryos, but were reduced by BGP-15 treatment (p<0.05). MMP and mtDNA copy number in the embryos generated from the H2O2-treated COCs were decreased compared to the control (p<0.05). BGP-15 did not alter MMP, but was able to restore mtDNA copy number in these embryos. These results demonstrate that COCs are acutely responsive to OS which impairs cleavage rates as well as embryo differentiation potentially via effects on mitochondria. Importantly, BGP-15, a drug currently in human clinical trials, is able to alleviate the effects of OS in oocytes and improve embryo development.