The Requirement for Transmembranal Electron Flow for Cell Proliferation
Diferric transferrin or other iron complexes have long been recognized as essential for cellular growth1–5. This requirement is primarily based on the essential role of iron in heme and DNA synthesis6,7. Removal of iron from cells inhibits growth8. The iron monement into the cell may depend on endocytosis of ferric transferrin attached to transferrin receptor in the plasma membrane9 or ferric iron uptake directly through the membrane by undefined transport systems5,10. Ferric chelates have also been used in place of transferrin to stimulate growth4,11. The discovery of an electron transport system in the plasma membrane which could reduce ferric chelates as well as other impermeable oxidants12,13 introduced a mechanism for ferric iron reduction outside the membrane before transport as ferrous iron. The discovery that impermeable ferricyanide stimulated cell growth under serum deficient conditions introduced a possible new role for ferric compounds as external oxidants to stimulate cell proliferation13,14. Since it has been shown that ferricyanide cannot stimulate growth of L1210 cells after iron depletion by desferrioxamine and cannot act as an iron supply for these cells5 we examined its effect on growth of cells which had not been depleted of iron.
KeywordsL1210 Cell Ribonucleotide Reductase Ferric Ammonium Sulfate Ferric Ammonium Citrate External Oxidant
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