Altered gut microbiome is strongly associated with the development of pathophysiological diseases mediated by oxidative stress (OS) in humans and animals. Hence, the aim of this thesis is to get a deeper understanding of the relationship between the gut microbiota and redox homeostasis caused by excessive intake of heavy metals (HM, Fe and Al) and exposure to inhalation anesthetics (IA) through monitoring of structural and functional changes of the gut microbiome, the intestinal barrier, OS, inflammation, regulation of hepcidin and ferritin, macrophage polarization and functional changes in tissues and organs. The results indicate that subacute and especially chronic administration of IA (sevoflurane/isoflurane) with excessive HM intake disrupts cellular metabolism. It further leads to disruption of essential metals and accumulation of HM, increased OS, inflammation, macrophage polarization, immune suppression, and dysbiosis associated with altered abundance and diversity of the gut microbiome, inflammation, altered levels of zonulin, serotonin, microbiota enzymes and absorption of micronutrients. Hepcidin level is closely related to macrophage polarization, OS, inflammation, and reorganization of damaged tissue, while ferritin as an inflammatory marker is increased in the presence of HM and/or IA. Isoflurane alone or in the presence of HM causes greater tissue damage compared to sevoflurane. Our data emphasize the molecular biological basis of understanding of the connection between IA, HM, gut microbiome, and macrophage polarization in order to undertake better therapeutic or preventive options to protect the patient from possible adverse consequences caused by excessive intake of IA, HM, and OS.