Impaired proliferation and DNA synthesis of a human tumor cell line (HELA)caused by short treatment with the antianemic drug jectofer (ferric-sorbitol-citrate) and the lipid peroxidation product 4-hydroxynonenal

Anti-anaemic drug, ferric-sorbitol-citrate complex (FSC), inhibit tumour ce ll growth through the mechanisms which are complex and not entirely underst ood, The probable mechanisms of described effects of iron is iron-induced o xidative stress of the treated cells. Hence, the effects of FSC on HeLa cel l growth in vitro were compared with the biological activity of one of the major mediators of the oxygen free radicals - aldehyde 4-hydroxinonenal (HN E), to see if the effects of FSC and of HNE resemble each other. Impaired p roliferative ability and DNA synthesis of HeLa cells was observed after tre atment with anti-anaemic drug FSC for 24 hours. After treatment with FSC an d culturing of HeLa cells in fresh medium for 24 or 96 hours the cells did not proliferate at all, DNA synthesis was transiently recovered and then di minished again. HNE blocked cell proliferation during the time the aldehyde was present in culture and 24 h later. Afterwards, the cells proliferated as control nontreated cells. HNE did not inhibit DNA synthesis during treat ment, bur intensity of H-3-thymidine incorporation was lower after preincub ation. Thus, both FSC and HNE interfere with the basic mechanisms of the ce ll growth regulation, while antitumour activity of FSC resembles, but does not necessarily include iron induced lipid peroxidation.