Review Article

Roles of Oxidative Stress in Polycystic Ovary Syndrome and Cancers

Figure 1

Interactions of oxidative stress, inflammation, insulin resistance, and hyperandrogenemia are described briefly in the figure, which are all involved in polycystic ovary syndrome physiopathology. Oxidative stress seems to induce cancer through genetic variation and cell signaling pathway. FFA, free fatty acid; ROS, reactive oxygen species; NF-κB, nuclear factor kappa B; AP-1, activator protein-1; HIF-1, hypoxia-induced factor-1; TNF-α, tumor necrosis factor-α; Nox, nicotinamide adenine dinucleotide phosphate oxidase system; IL, interleukin; JNK, c-Jun N-terminal kinase; InsR, insulin receptor; IRS, insulin receptor substrate; Tyr Phos, tyrosine phosphorylation; Ser Phos, serine phosphorylation; PI3K, phosphatidyl inositol 3-kinase; Akt, protein kinase B; GLUT4, glucose transporter-4; GnRH, gonadotropin-releasing hormone; LH, luteinizing hormone; SHBG, sex hormone-binding globulin; IGFBP-1, insulin growth factor binding protein; IGF-1, insulin growth factor-1.