In humans, errors in meiotic chromosome segregation that produce aneuploid gametes increase dramatically as women age, a phenomenon termed the maternal age effect. During meiosis, cohesion between sister chromatids keeps recombinant homologs physically attached and premature loss of cohesion can lead to missegregation of homologs during meiosis I. A growing body of evidence suggests that meiotic cohesion deteriorates as oocytes age and contributes to the maternal age effect. One hallmark of aging cells is an increase in oxidative damage caused by reactive oxygen species (ROS). Therefore, increased oxidative damage in older oocytes may be one of the factors that lead to premature loss of cohesion and segregation errors. To test this hypothesis we used a Gal4/UAS RNAi strategy to induce oxidative stress in Drosophila oocytes and measured the fidelity of chromosome segregation during meiosis. Knockdown of the ROS scavengers SOD1 (cytoplasmic) or SOD2 (mitochondrial) caused a significant increase in segregation errors. This increase occurred primarily because recombinant chromosomes missegregated during meiosis I at a significantly greater frequency, consistent with oxidative damage causing premature loss of meiotic cohesion. FISH analysis confirmed that arm cohesion is disrupted in SOD knockdown genotypes. Together these results provide the first in vivo demonstration that oxidative stress during meiotic prophase induces chromosome segregation errors and support the model that accelerated loss of cohesion in aging human oocytes is caused, at least in part, by oxidative damage.