The monovalent reduction of molecular oxygen, resulting in the formation of superoxide radicals (O(2)) is regarded as to be an ongoing physiological process involved in the respiration and other biological processes of aerobic cells. These reactive oxygen species have been reported to function as cofactors in many biosynthetic reaction steps. Thus, deviations from cellular steady state concentrations may lead to a multiplicity of clinical symptoms or may to a great deal determine the characteristic of a distinct malady. Decrease of cellular O(2)-concentration is discussed in connection with Trisomie 21 and various mental disorders. The role of O(2) in the biochemistry of inflammation, autoimmune diseases, various toxicological cases and the biological aging process is described. Hypothetical considerations concerning the involvement of O(2) in the pathogenetic mechanisms of Morbus Wilson, haemochromatosis, Parkinson syndrome, cataractogenesis and in carcinogenesis are presented. The physiological control of cellular O(2)-concentration is performed by formation rates of the various cellular O(2)-sources and the overall elimination rates of O(2)-consuming reaction steps. Superoxide dismutase (SOD) is of special interest within this cycle because it detoxifies O(2) radicals with velocity rates which are significantly faster than any other pathway involved in O(2) elimination. Thus attempts for a therapeutic interference on tissue levels of O(2)-radicals are mainly based on inhibition or activation of cellular SOD-activities depending on a supposed decrease or increase in cellular steady state concentrations of O(2). The availability of a drug version of SOD and of various synthetic SOD-active compounds allowing a therapeutic decrease of O(2)-tissue levels. Inhibition of cellular SOD is also possible, however, many still unknown toxic side effects should be expected because of unspecific action of the inhibitor available.