The thesis investigates the effect of inhaled anaesthetics in the presence of iron on the prooxidative/antioxidant effects of peripheral tissues and organs in chronic inflammation. It intends to understand how excessive iron intake alters physiological, functional characteristics of peripheral tissues and whether different anaesthetics can alter cell metabolism regarding transition metals as initiators of reactive oxygen species (ROS) and inflammation through regulation of hepcidin, transferrin, and macrophage polarization. Y59 rats were injected intraperitoneally (ip) a solution of iron dextran at a dose of 50 mg/kg or were exposed to inhaled anaesthetics sevoflurane (2.4%) and isoflurane (1.3%) and the combination for 28 days every other day. The results show that anaesthetics reduce the rat's body weight and increase oxidative stress (OS) in peripheral tissues, leading to M1 macrophage polarization. Excessive iron intake leads to iron accumulation in peripheral tissues, an increase in OS and inflammation, and an increase in the ratio of IL-12/IL-10 cytokines to the M1 macrophage phenotype. The combination of sevoflurane and iron accumulates iron in tissues, showing iron's protective effect and the M2 phenotype of macrophages. The combination of iron dextran and isoflurane in rats leads to hypoxia, increased iron release from macrophages of the reticuloendothelial system and increased erythropoiesis. Hepcidin levels in the liver are regulated by a complex interreaction of inflammation, oxidative stress, free iron levels, erythropoiesis and hypoxia.