Effect of iron chelators on proliferation and iron uptake in hepatoma cells

Kicic, Anthony; Chua, Anita; Baker, Erica

doi:10.1002/1097-0142(20011215)92:12<3093::aid-cncr10107>3.0.co;2-b

Cited by 67 publications

(59 citation statements)

References 34 publications

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“…We analyzed how iron chelators with different membrane permeabilities altered the H 2 O 2 hypersensitivity of D282⌬dpr. The hydrophilic iron chelator DFOM, a siderophore produced by Streptomyces pilosus, has been used in several studies to interfere with the intracellular iron pool of both prokaryotic and eukaryotic cells (43)(44)(45)(46). DTPA, on the other hand, has been used as an extracellular iron chelator (46).…”

Section: Resultsmentioning

confidence: 99%

Molecular Basis of H2O2 Resistance Mediated by Streptococcal Dpr

Pulliainen

Haataja

Kähkönen

et al. 2003

Journal of Biological Chemistry

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Section: Resultsmentioning

confidence: 99%

Molecular Basis of H2O2 Resistance Mediated by Streptococcal Dpr

Pulliainen

Haataja

Kähkönen

et al. 2003

Journal of Biological Chemistry

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“…These studies can also contribute in research related to cancer, because iron is essential for proliferation of cancer cells (Kicic et al 2001).…”

Section: Ironmentioning

confidence: 99%

Iron transportation across the placenta

Oliveira

Rodrigues

Miglino

2012

An. Acad. Bras. Ciênc.

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According to the classification of placental types among animals, the transfer of iron through the placenta can occur via: absorption connected to transferin through the outer surface of the trophoblast in direct contact with circulating maternal blood; absorption of the erythrocytes by the chorionic epithelium in direct contact with accumulation of blood extravased from haemotophagous areas; absorption by the chorionic epithelium in direct contact with iron enriched secretions from the endometrial glands and absorption by extravasations of the blood in the maternal-fetal surface and the subsequent phagocytosis of the erythrocytes by trophoblast cells described in bovine, small ruminants, canine and feline. The function of erythrophagocytosis observed after the extravasation of blood in the maternal-fetal interface is undefined in several species. Possibly, the iron is transferred to the fetus through the trophoblastic erythrophagocytosis in the hemophogous area of the placenta and also in the endometrial glands. In this literature survey, new methods of studies regarding placental transfer involving iron and other nutrients necessary for survival and maintenance of embryonic fetus to birth are proposed.

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“…To test this we utilized a highly specific membrane-permeable ferric iron chelator, DFO, which have been shown to deplete intracellular pools of free iron (53)(54)(55). Results of immunocytochemistry (Fig.…”

Section: Low and High Doses Of Iron Produce Opposite Effects Onmentioning

confidence: 99%

Fluctuations of Intracellular Iron Modulate Elastin Production

Bunda

Kaviani

Hinek

2005

Journal of Biological Chemistry

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Production of insoluble elastin, the major component of elastic fibers, can be modulated by numerous intrinsic and exogenous factors. Because patients with hemolytic disorders characterized with fluctuations in iron concentration demonstrate defective elastic fibers, we speculated that iron might also modulate elastogenesis. In the present report we demonstrate that treatment of cultured human skin fibroblasts with low concentration of iron 2-20 M (ferric ammonium citrate) induced a significant increase in the synthesis of tropoelastin and deposition of insoluble elastin. Northern blot and realtime reverse transcription-PCR analysis revealed that treatment with 20 M iron led to an increase of ϳ3-fold in elastin mRNA levels. Because treatment with an intracellular iron chelator, desferrioxamine, caused a significant decrease in elastin mRNA level and consequent inhibition of elastin deposition, we conclude that iron facilitates elastin gene expression. Our experimental evidence also demonstrates the existence of an opposite effect, in which higher, but not cytotoxic concentrations of iron (100 -400 M) induced the production of intracellular reactive oxygen species that coincided with a significant decrease in elastin message stability and the disappearance of iron-dependent stimulatory effect on elastogenesis. This stimulatory elastogenic effect was reversed, however, in cultures simultaneously treated with high iron concentration (200 M) and the intracellular hydroxyl radical scavenger, dimethylthiourea. Thus, presented data, for the first time, demonstrate the existence of two opposite iron-dependent mechanisms that may affect the steady state of elastin message. We speculate that extreme fluctuations in intracellular iron levels result in impaired elastic fiber production as observed in hemolytic diseases.Mature elastic fibers and laminae provide extensibility and elastic recoil to vascular walls and ligaments and form a connective tissue framework of lungs, elastic cartilage, and skin (1, 2). They are complex structures made of polymeric (insoluble) elastin and 12-nm microfibrils that consist of several glycoproteins, e.g. fibrillins, fibulins, and microfibril-associated glycoproteins (3-6). Elastic fiber formation (elastogenesis) is a complex process involving several intracellular and extracellular events. Cells (fibroblasts, endothelial cells, chondroblasts, or vascular smooth muscle cells) must first synthesize and secrete numerous glycoproteins to form a microfibrillar scaffold upon which tropoelastin, the precursor peptides, are properly assembled and covalently cross-linked by lysyl oxidase into a resilient polymer, insoluble elastin (7-10). Production of elastin reaches its highest levels in the third trimester of the fetal life and steadily decreases during early postnatal development (11,12). In undisturbed tissues, elastic fibers may last over the entire human lifespan (13,14).The net deposition of elastin appears to be controlled on both the transcriptional level (tropoelastin mRNA message express...

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Effect of iron chelators on proliferation and iron uptake in hepatoma cells

Cited by 67 publications

References 34 publications

Molecular Basis of H2O2 Resistance Mediated by Streptococcal Dpr

Molecular Basis of H2O2 Resistance Mediated by Streptococcal Dpr

Iron transportation across the placenta

Fluctuations of Intracellular Iron Modulate Elastin Production

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