Hepatitis of any kind is characterized by increased concentrations of reactive oxygen species. H2O2 is the main reactive oxygen intermediate derived from a multitude of cellular metabolic processes as well as from oxidative burst by granulocytes or macrophages. Due to its relatively long half-life time, there is growing evidence that H2O2 also acts as a signaling molecule. Iron metabolism can be influenced by H2O2 by activating the iron regulatory protein 1, which regulates intracellular iron metabolism but also by increasing transferrin receptor 1 that is responsible for cellular iron uptake. Both mechanisms lead to increased cellular iron uptake and decreased levels of circulating serum iron. Hepcidin, the systemic iron regulator, has not been linked to oxidative stress so far. New experiments, however, point out that H2O2 is able to increase hepcidin via STAT3 signaling, thus decreasing iron recycling by macrophages and iron resorption by the duodenum. This is a third mechanism to lower serum iron during increased oxidative stress and preventing toxic reactions between H2O2 and iron.