Poor oocyte quality is a leading cause of reduced fertility in humans and animals. However, the factors underpinning oocyte quality are poorly understood. Studies in several species have shown that during oocyte growth and maturation an increasing proportion of mitochondria become hooded, but the purpose of this structural change is unknown. We have also observed differences in the timing of this morphological change between good and poor quality oocytes in a sheep model [1]. The aim of our research is to understand how mitochondrial structure, function and oocyte quality are interconnected to identify novel ways of modifying oocyte quality. Adult sheep oocytes were treated with the mitochondrial inhibitors, FCCP, oligomycin and antimycin A for one hour at the start of in vitro maturation. Changes to the number of hooded mitochondria and mitochondrial membrane potential (MMP) were measured using transmission electron microscopy and confocal microscopy with TMRM staining. Oocytes treated with the electron transport chain uncoupler, FCCP, had decreased mean fluorescent intensity (P = 0.0046) and a trend towards an increased proportion of hooded mitochondria (P = 0.0626) compared to those treated with the vehicle control. In contrast, oligomycin (ATP synthase inhibitor) treatment decreased the percentage of hooded mitochondria (P = 0.0287) but had variable effects on oocyte MMP. Antimycin A had no effect on either the proportion of hooded mitochondria or MMP. These results support our hypothesis that the increased proportion of hooded mitochondria observed after oocyte maturation represents an increase in the uncoupling of the electron transport chain. Our continuing research will determine if altering mitochondrial structure and function can alter oocyte quality using in vitro embryo production techniques. This may lead to the development of modified in vitro maturation media that can improve oocyte quality.