Polycystic ovary syndrome (PCOS) is the most common ovulatory disorder in the world and is associated with multiple adverse outcomes. The phenotype is widely varied, with several pathologies contributing to the spectrum of the disease including insulin resistance, obesity and hyperandrogenemia. Of these, the role of hyperandrogenemia and the mechanism by which it causes dysfunction remains poorly understood. Early studies have shown that androgens may affect the metabolic pathways of a cell, and this may pose hazards at the level of the mitochondria. As mitochondria are strictly maternally inherited, this would provide an exciting explanation not only to the pathophysiology of PCOS as a disease, but also to the inheritance pattern. This review seeks to summarize what is known about PCOS and associated adverse outcomes with focus on the role of hyperandrogenemia and specific emphasis on the oocyte.