Effects of Iron Chelates on the Transferrin-Free Culture of Rat Dermal Fibroblasts through Active Oxygen Generation

Effects of nonchelating and chelating agents at 10 mM on the serum-free culture of rat dermal fibroblasts were investigated. A strong iron-chelating agent, iminodiacetic acid (IDA), and a weak one, dihydroxyethylglycine (DHEG), decreased iron permeation into preconfluent fibroblasts. A weak iron-che...

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Veröffentlicht in:In vitro cellular & developmental biology. Animal 1997-07, Vol.33 (7), p.527-535
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description Effects of nonchelating and chelating agents at 10 mM on the serum-free culture of rat dermal fibroblasts were investigated. A strong iron-chelating agent, iminodiacetic acid (IDA), and a weak one, dihydroxyethylglycine (DHEG), decreased iron permeation into preconfluent fibroblasts. A weak iron-chelating agent, glycylglycine (GG), a nonchelating agent, N-2-hydroxyethylpiperazine -N'-2-ethanesulfonic acid (HEPES), and human apotransferrin ($10 \mug/ml$) increased the permeation with time. Iron may be essential for survival of fibroblasts because subconfluent fibroblasts exposed to$100 \muM FeSO_4$in combination with transferrin, HEPES, or GG significantly decreased to release lactate dehydrogenase into the medium. Superoxide dismutase and dimethyl sulfoxide blocked the enzyme release, suggesting that Superoxide and hydroxyl radical induce cellular damage but hydrogen peroxide (H2O 2) generated by Superoxide dismutation does not. GG significantly reduced H2O 2cytotoxicity. DHEG acted as a potent promoter of the iron-stimulated cellular damage if ascorbate or H2O 2was added to the medium. FeSO4and FeCl3(50 to$100 \muM$) individually combined with IDA maximally promoted fibroblast proliferation. Ascorbate increased formation of thiobarbituric acid-reactive substances from deoxyribose in the medium supplemented with FeSO4and either IDA or DHEG. Conversely, ascorbate decreased the formation in the medium with FeSO4and with or without other agents. Fibroblast proliferation may thus be stimulated through the active oxygen generation mediated by a redox-cycling between Fe3+and Fe2+, which are dissolved in the medium at a high concentration, rather than through delivery of iron into the cells.
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A strong iron-chelating agent, iminodiacetic acid (IDA), and a weak one, dihydroxyethylglycine (DHEG), decreased iron permeation into preconfluent fibroblasts. A weak iron-chelating agent, glycylglycine (GG), a nonchelating agent, N-2-hydroxyethylpiperazine -N'-2-ethanesulfonic acid (HEPES), and human apotransferrin ($10 \mug/ml$) increased the permeation with time. Iron may be essential for survival of fibroblasts because subconfluent fibroblasts exposed to$100 \muM FeSO_4$in combination with transferrin, HEPES, or GG significantly decreased to release lactate dehydrogenase into the medium. Superoxide dismutase and dimethyl sulfoxide blocked the enzyme release, suggesting that Superoxide and hydroxyl radical induce cellular damage but hydrogen peroxide (H2O 2) generated by Superoxide dismutation does not. GG significantly reduced H2O 2cytotoxicity. DHEG acted as a potent promoter of the iron-stimulated cellular damage if ascorbate or H2O 2was added to the medium. FeSO4and FeCl3(50 to$100 \muM$) individually combined with IDA maximally promoted fibroblast proliferation. Ascorbate increased formation of thiobarbituric acid-reactive substances from deoxyribose in the medium supplemented with FeSO4and either IDA or DHEG. Conversely, ascorbate decreased the formation in the medium with FeSO4and with or without other agents. 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Animal</title><addtitle>In Vitro Cell Dev Biol Anim</addtitle><description>Effects of nonchelating and chelating agents at 10 mM on the serum-free culture of rat dermal fibroblasts were investigated. A strong iron-chelating agent, iminodiacetic acid (IDA), and a weak one, dihydroxyethylglycine (DHEG), decreased iron permeation into preconfluent fibroblasts. A weak iron-chelating agent, glycylglycine (GG), a nonchelating agent, N-2-hydroxyethylpiperazine -N'-2-ethanesulfonic acid (HEPES), and human apotransferrin ($10 \mug/ml$) increased the permeation with time. Iron may be essential for survival of fibroblasts because subconfluent fibroblasts exposed to$100 \muM FeSO_4$in combination with transferrin, HEPES, or GG significantly decreased to release lactate dehydrogenase into the medium. Superoxide dismutase and dimethyl sulfoxide blocked the enzyme release, suggesting that Superoxide and hydroxyl radical induce cellular damage but hydrogen peroxide (H2O 2) generated by Superoxide dismutation does not. GG significantly reduced H2O 2cytotoxicity. DHEG acted as a potent promoter of the iron-stimulated cellular damage if ascorbate or H2O 2was added to the medium. FeSO4and FeCl3(50 to$100 \muM$) individually combined with IDA maximally promoted fibroblast proliferation. Ascorbate increased formation of thiobarbituric acid-reactive substances from deoxyribose in the medium supplemented with FeSO4and either IDA or DHEG. Conversely, ascorbate decreased the formation in the medium with FeSO4and with or without other agents. 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A weak iron-chelating agent, glycylglycine (GG), a nonchelating agent, N-2-hydroxyethylpiperazine -N'-2-ethanesulfonic acid (HEPES), and human apotransferrin ($10 \mug/ml$) increased the permeation with time. Iron may be essential for survival of fibroblasts because subconfluent fibroblasts exposed to$100 \muM FeSO_4$in combination with transferrin, HEPES, or GG significantly decreased to release lactate dehydrogenase into the medium. Superoxide dismutase and dimethyl sulfoxide blocked the enzyme release, suggesting that Superoxide and hydroxyl radical induce cellular damage but hydrogen peroxide (H2O 2) generated by Superoxide dismutation does not. GG significantly reduced H2O 2cytotoxicity. DHEG acted as a potent promoter of the iron-stimulated cellular damage if ascorbate or H2O 2was added to the medium. FeSO4and FeCl3(50 to$100 \muM$) individually combined with IDA maximally promoted fibroblast proliferation. Ascorbate increased formation of thiobarbituric acid-reactive substances from deoxyribose in the medium supplemented with FeSO4and either IDA or DHEG. Conversely, ascorbate decreased the formation in the medium with FeSO4and with or without other agents. Fibroblast proliferation may thus be stimulated through the active oxygen generation mediated by a redox-cycling between Fe3+and Fe2+, which are dissolved in the medium at a high concentration, rather than through delivery of iron into the cells.</abstract><cop>Germany</cop><pub>Society for In Vitro Biology</pub><pmid>9282313</pmid><doi>10.1007/s11626-997-0095-1</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record>
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source MEDLINE; SpringerNature Journals; JSTOR Archive Collection A-Z Listing
subjects Animals
Antioxidants
Antioxidants - pharmacology
Apoproteins - pharmacology
Apotransferrin
Ascorbic acid
Cell aggregates
Cell culture
Cell Division - drug effects
Cells, Cultured
Cellular Models
Chelates
Chelating agents
Chelation
Culture
Cytotoxicity
Damage
Dimethyl sulfoxide
Dimethyl Sulfoxide - pharmacology
Ferric chloride
Ferrous Compounds - pharmacology
Fibroblasts
Fibroblasts - drug effects
Fibroblasts - metabolism
Glycine - analogs & derivatives
Glycine - pharmacology
Glycylglycine - pharmacology
Humans
Hydrogen peroxide
Hydrogen Peroxide - metabolism
Hydrogen Peroxide - pharmacology
Hydroxyl radicals
Imino acids
Imino Acids - pharmacology
Iminodiacetic acid
Iron
Iron chelating agents
Iron Chelating Agents - pharmacology
Iron deficiency anemia
Iron sulfates
L-Lactate dehydrogenase
L-Lactate Dehydrogenase - metabolism
Lactate dehydrogenase
Lactic acid
Lipids
Male
Metal aggregates
Oxygen
Oxygen - metabolism
Penetration
Rats
Rats, Wistar
Reactive oxygen species
Redox properties
Superoxide dismutase
Superoxide Dismutase - pharmacology
Superoxides
Thiobarbituric acid
Thiobarbituric Acid Reactive Substances - metabolism
Toxicity
Transferrin
Transferrin - pharmacology
Transferrin - physiology
Transferrins
title Effects of Iron Chelates on the Transferrin-Free Culture of Rat Dermal Fibroblasts through Active Oxygen Generation
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