Oocyte quality deteriorates markedly with ageing leading to disordered spindle assembly and reduced defense against deleterious reactive oxygen species (ROS). Sirtuins are a family of seven (SIRT1-7) NAD+-dependent deacetylases with potent anti-ageing properties. We recently showed that in somatic cells, SIRT2 stabilizes Budding uninhibited by benzimidazole-Related 1 (BubR1), which we previously showed controls oocyte spindle assembly and declines with ageing in oocytes. Here we studied oocytes from a transgenic mouse that overexpresses SIRT2 (SIRT2-Tg mice). BubR1 was increased in SIRT2-Tg oocytes pointing to SIRT2-dependent BubR1 stabilization as in somatic cells. To determine whether SIRT2 overexpression would impact oocyte quality during natural ageing, we aged mice to 12 months when oocyte quality is known to be poor. We first examined in vitro meiotic maturation, which commences with germinal vesicle breakdown (GVBD) and concludes with first polar body extrusion (PBE). Interestingly, by 16 h post-GVBD, almost twice as many aged SIRT2-Tg oocytes underwent PBE compared with WT (69% versus 36%; P=0.04), comparable to PBE rates observed in younger (4-month-old) WT oocytes (62%). Thus, SIRT2 overexpression reverses poor meiotic competence brought on by ageing. Strikingly, aged SIRT2-Tg oocytes also exhibited higher rates of normal spindles with aligned chromosomes both in meiosis I (70% versus 15%) and at metaphase II-arrest (44% versus 25%). Finally, following hydrogen-peroxide-induced oxidative stress, ROS levels in SIRT2-Tg oocytes were less than half that in WT oocytes (P<0.0001) indicating that SIRT2 overexpression potentiates anti-oxidant defenses. Collectively, these data show that SIRT2 combats age-induced deterioration in oocyte quality. Two possible mechanisms could involve increased BubR1 stability and enhanced capacity for ROS detoxification. Approaches for increasing SIRT2 activity could therefore provide an attractive avenue for modulating oocyte quality.