Iron and/or
ferritin accumulation are known to occur under pathological conditions in many inflammatory
skin diseases or in human skin chronically exposed to UV light. Under such conditions,
ferritin is believed to play an effective protective role in accommodating and 'deactivating' excess 'free'
iron produced by the inflammatory process or the UV illumination. The present study compares the relationship between
ferritin over-expression and effects of an oxidative stress induced chemically by
tert-butyl hydroperoxide or photochemically by UV-A radiation. As shown by immunoassay, cultured MRC 5 and HS 68 fibroblasts treated for at least one day with
transferrin or overnight with non-toxic concentrations of the
ferric nitrilotriacetate complex express up to 10 times more
ferritin than untreated cells, whereas a five-fold increase is obtained with NCTC 2544 keratinocytes. In all cases a parallel increase in soluble cellular
iron is measured by inductive plasma emission spectroscopy. The
superoxide dismutase and
catalase activities and total
glutathione levels are not modified by the
iron treatment, whereas a transient increase in the Se-dependent
glutathione peroxidase activity of keratinocytes is observed after a short incubation with the
iron complex. In keratinocytes and fibroblasts,
ferritin over-expression after
iron treatment markedly inhibits lipid peroxidation but, paradoxically, not the mortality induced by
tert-butyl hydroperoxide. In contrast, this excess
ferritin does not protect cells from both the peroxidation and mortality induced by moderate doses (30 J/cm2) of UV-A radiation. As a consequence, protection against oxidative damage by excess
ferritin synthesis clearly depends on the nature of the oxidative stress on cell targets and it seems to be of lesser importance in the case of photochemically induced oxidation.