epidermal-growth-factor has been researched along with bathophenanthroline-disulfonic-acid* in 2 studies
2 other study(ies) available for epidermal-growth-factor and bathophenanthroline-disulfonic-acid
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Iron reverses impermeable chelator inhibition of DNA synthesis in CCl 39 cells.
Treatment of Chinese hamster lung fibroblasts (CCl 39 cells) with the impermeable iron(II) chelator bathophenanthroline disulfonate (BPS) inhibits DNA synthesis when cell growth is initiated with growth factors including epidermal growth factor plus insulin, thrombin, or ceruloplasmin, but not with 10% fetal calf serum. The BPS treatment inhibits transplasma membrane electron transport. The treatment leads to release of iron from the cells as determined by BPS iron(II) complex formation over 90 min. Growth factor stimulation of DNA synthesis and electron transport are restored by addition of di- or trivalent iron to the cells in the form of ferric ammonium citrate, ferrous ammonium sulfate, or diferric transferrin. The effect with BPS differs from the inhibition of growth by hydroxyurea, which acts on the ribonucleotide reductase, or diethylenetriaminepentaacetic acid, which is another impermeable chelating agent, in that these agents inhibit growth in 10% fetal calf serum. The BPS effect is consistent with removal of iron from a site on the cell surface that controls DNA synthesis. Topics: Animals; Cations, Divalent; Cell Line; Chelating Agents; Cricetinae; Cricetulus; DNA; DNA Replication; Electron Transport; Epidermal Growth Factor; Hydroxyurea; Iron; Kinetics; Lung; Pentetic Acid; Phenanthrolines; Thymidine | 1994 |
Iron at the cell surface controls DNA synthesis in CCl 39 cells.
Treatment of CCl 39 cells with the impermeable iron II chelator bathophenanthroline disulfonate (BPS) inhibits both DNA synthesis and transplasma membrane electron transport. The inhibition persists when the BPS is removed, and the extract from 10(6) cells contains up to 1.28 nmoles iron II chelated to BPS. The BPS iron II chelate itself is not inhibitory. Both DNA synthesis and electron transport are restored by addition of microM iron II or iron III compounds to extracted cells. Other impermeable chelators for iron II give similar inhibition, whereas the iron III-specific Tiron or copper-specific bathocuproine sulfonate do not inhibit. The inhibition differs from the permeable iron III chelator inhibition of ribonucleotide reductase, because inhibition of DNA synthesis by the permeable chelators is reversed when chelator is removed. The response to growth factors also differs, with no impermeable chelator inhibition on 10% fetal calf serum contrasting to inhibition by permeable chelators. DNA synthesis with both activation of tyrosine kinase with EGF plus insulin or by thrombin or ceruloplasmin led to protein kinase C activation as inhibited by the impermeable chelators. It is proposed that an iron available on the cell surface is required for DNA synthesis and plasma membrane electron transport. Topics: Animals; Apoproteins; Cations, Divalent; Cell Line; Cell Membrane; Cricetinae; Cricetulus; DNA; DNA Replication; Electron Transport; Epidermal Growth Factor; Fibroblasts; Insulin; Iron; Iron Chelating Agents; Kinetics; Lung; Phenanthrolines; Thymidine; Transferrin; Tritium | 1994 |