Research group overviewOwing to its significant redox potential and its ability to readily alternate between reduced and oxidized states, iron easily associates with proteins, binds to oxygen, transfers electrons and mediates catalytic reactions. Accordingly, iron is used by different types of cells as a cofactor in oxygen transport, energy cycling and DNA synthesis among other metabolic processes. Under aerobic conditions though, free iron leads to increased oxidative stress through Fenton chemistry which propagates reactive oxygen species (ROS) and generates highly reactive hydroxyl radicals. Oxidative stress damages macromolecules, injures tissues, and predisposes to cancer and cardiovascular complications among other diseases. The identification of several proteins involved in iron metabolism in recent years has revived the field of iron biology. Currently, basic research focusing on the interplay between various regulatory proteins involved in iron homeostasis and how iron homeostasis could be disrupted in different disease states like cancer is a topic of great interest. Furthermore, with the advent of these discoveries, research work aiming to understand the role of iron in the pathogenesis of cancer and other diseases is gaining significant momentum. Several lines of evidence, including work done in our lab, suggest that estrogen (17-β estradiol) manipulates iron homeostasis by down-regulating the synthesis of hepcidin, the major iron regulator in mammalian systems. This maintains ferroportin (FPN) integrity and sustains iron efflux from cells into the circulation. One implication of this critical observation is that iron could function as a translator of some of the biological effects of estrogen in health and disease. Such an estrogen-iron axis can lend itself to further investigating several longstanding paradoxes in estrogen biology.