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Labile plasma iron in iron overload: redox activity and susceptibility to chelation
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| Zeitschriftentitel: | Blood |
|---|---|
| Personen und Körperschaften: | , , , , , |
| In: | Blood, 102, 2003, 7, S. 2670-2677 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
American Society of Hematology
|
| Schlagwörter: |
| author_facet |
Esposito, Breno P. Breuer, William Sirankapracha, Pornpan Pootrakul, Pensri Hershko, Chaim Cabantchik, Z. Ioav Esposito, Breno P. Breuer, William Sirankapracha, Pornpan Pootrakul, Pensri Hershko, Chaim Cabantchik, Z. Ioav |
|---|---|
| author |
Esposito, Breno P. Breuer, William Sirankapracha, Pornpan Pootrakul, Pensri Hershko, Chaim Cabantchik, Z. Ioav |
| spellingShingle |
Esposito, Breno P. Breuer, William Sirankapracha, Pornpan Pootrakul, Pensri Hershko, Chaim Cabantchik, Z. Ioav Blood Labile plasma iron in iron overload: redox activity and susceptibility to chelation Cell Biology Hematology Immunology Biochemistry |
| author_sort |
esposito, breno p. |
| spelling |
Esposito, Breno P. Breuer, William Sirankapracha, Pornpan Pootrakul, Pensri Hershko, Chaim Cabantchik, Z. Ioav 0006-4971 1528-0020 American Society of Hematology Cell Biology Hematology Immunology Biochemistry http://dx.doi.org/10.1182/blood-2003-03-0807 <jats:title>Abstract</jats:title> <jats:p>Plasma non-transferrin-bound-iron (NTBI) is believed to be responsible for catalyzing the formation of reactive radicals in the circulation of iron overloaded subjects, resulting in accumulation of oxidation products. We assessed the redox active component of NTBI in the plasma of healthy and β-thalassemic patients. The labile plasma iron (LPI) was determined with the fluorogenic dihydrorhodamine 123 by monitoring the generation of reactive radicals prompted by ascorbate but blocked by iron chelators. The assay was LPI specific since it was generated by physiologic concentrations of ascorbate, involved no sample manipulation, and was blocked by iron chelators that bind iron selectively. LPI, essentially absent from sera of healthy individuals, was present in those of β-thalassemia patients at levels (1-16 μM) that correlated significantly with those of NTBI measured as mobilizer-dependent chelatable iron or desferrioxamine chelatable iron. Oral treatment of patients with deferiprone (L1) raised plasma NTBI due to iron mobilization but did not lead to LPI appearance, indicating that L1-chelated iron in plasma was not redox active. Moreover, oral L1 treatment eliminated LPI in patients. The approach enabled the assessment of LPI susceptibility to in vivo or in vitro chelation and the potential of LPI to cause tissue damage, as found in iron overload conditions. (Blood. 2003;102:2670-2677)</jats:p> Labile plasma iron in iron overload: redox activity and susceptibility to chelation Blood |
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10.1182/blood-2003-03-0807 |
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American Society of Hematology, 2003 |
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| title |
Labile plasma iron in iron overload: redox activity and susceptibility to chelation |
| title_unstemmed |
Labile plasma iron in iron overload: redox activity and susceptibility to chelation |
| title_full |
Labile plasma iron in iron overload: redox activity and susceptibility to chelation |
| title_fullStr |
Labile plasma iron in iron overload: redox activity and susceptibility to chelation |
| title_full_unstemmed |
Labile plasma iron in iron overload: redox activity and susceptibility to chelation |
| title_short |
Labile plasma iron in iron overload: redox activity and susceptibility to chelation |
| title_sort |
labile plasma iron in iron overload: redox activity and susceptibility to chelation |
| topic |
Cell Biology Hematology Immunology Biochemistry |
| url |
http://dx.doi.org/10.1182/blood-2003-03-0807 |
| publishDate |
2003 |
| physical |
2670-2677 |
| description |
<jats:title>Abstract</jats:title>
<jats:p>Plasma non-transferrin-bound-iron (NTBI) is believed to be responsible for catalyzing the formation of reactive radicals in the circulation of iron overloaded subjects, resulting in accumulation of oxidation products. We assessed the redox active component of NTBI in the plasma of healthy and β-thalassemic patients. The labile plasma iron (LPI) was determined with the fluorogenic dihydrorhodamine 123 by monitoring the generation of reactive radicals prompted by ascorbate but blocked by iron chelators. The assay was LPI specific since it was generated by physiologic concentrations of ascorbate, involved no sample manipulation, and was blocked by iron chelators that bind iron selectively. LPI, essentially absent from sera of healthy individuals, was present in those of β-thalassemia patients at levels (1-16 μM) that correlated significantly with those of NTBI measured as mobilizer-dependent chelatable iron or desferrioxamine chelatable iron. Oral treatment of patients with deferiprone (L1) raised plasma NTBI due to iron mobilization but did not lead to LPI appearance, indicating that L1-chelated iron in plasma was not redox active. Moreover, oral L1 treatment eliminated LPI in patients. The approach enabled the assessment of LPI susceptibility to in vivo or in vitro chelation and the potential of LPI to cause tissue damage, as found in iron overload conditions. (Blood. 2003;102:2670-2677)</jats:p> |
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| author | Esposito, Breno P., Breuer, William, Sirankapracha, Pornpan, Pootrakul, Pensri, Hershko, Chaim, Cabantchik, Z. Ioav |
| author_facet | Esposito, Breno P., Breuer, William, Sirankapracha, Pornpan, Pootrakul, Pensri, Hershko, Chaim, Cabantchik, Z. Ioav, Esposito, Breno P., Breuer, William, Sirankapracha, Pornpan, Pootrakul, Pensri, Hershko, Chaim, Cabantchik, Z. Ioav |
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| description | <jats:title>Abstract</jats:title> <jats:p>Plasma non-transferrin-bound-iron (NTBI) is believed to be responsible for catalyzing the formation of reactive radicals in the circulation of iron overloaded subjects, resulting in accumulation of oxidation products. We assessed the redox active component of NTBI in the plasma of healthy and β-thalassemic patients. The labile plasma iron (LPI) was determined with the fluorogenic dihydrorhodamine 123 by monitoring the generation of reactive radicals prompted by ascorbate but blocked by iron chelators. The assay was LPI specific since it was generated by physiologic concentrations of ascorbate, involved no sample manipulation, and was blocked by iron chelators that bind iron selectively. LPI, essentially absent from sera of healthy individuals, was present in those of β-thalassemia patients at levels (1-16 μM) that correlated significantly with those of NTBI measured as mobilizer-dependent chelatable iron or desferrioxamine chelatable iron. Oral treatment of patients with deferiprone (L1) raised plasma NTBI due to iron mobilization but did not lead to LPI appearance, indicating that L1-chelated iron in plasma was not redox active. Moreover, oral L1 treatment eliminated LPI in patients. The approach enabled the assessment of LPI susceptibility to in vivo or in vitro chelation and the potential of LPI to cause tissue damage, as found in iron overload conditions. (Blood. 2003;102:2670-2677)</jats:p> |
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| imprint | American Society of Hematology, 2003 |
| imprint_str_mv | American Society of Hematology, 2003 |
| institution | DE-Pl11, DE-Rs1, DE-105, DE-14, DE-Ch1, DE-L229, DE-D275, DE-Bn3, DE-Brt1, DE-D161, DE-Zwi2, DE-Gla1, DE-Zi4, DE-15 |
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| spelling | Esposito, Breno P. Breuer, William Sirankapracha, Pornpan Pootrakul, Pensri Hershko, Chaim Cabantchik, Z. Ioav 0006-4971 1528-0020 American Society of Hematology Cell Biology Hematology Immunology Biochemistry http://dx.doi.org/10.1182/blood-2003-03-0807 <jats:title>Abstract</jats:title> <jats:p>Plasma non-transferrin-bound-iron (NTBI) is believed to be responsible for catalyzing the formation of reactive radicals in the circulation of iron overloaded subjects, resulting in accumulation of oxidation products. We assessed the redox active component of NTBI in the plasma of healthy and β-thalassemic patients. The labile plasma iron (LPI) was determined with the fluorogenic dihydrorhodamine 123 by monitoring the generation of reactive radicals prompted by ascorbate but blocked by iron chelators. The assay was LPI specific since it was generated by physiologic concentrations of ascorbate, involved no sample manipulation, and was blocked by iron chelators that bind iron selectively. LPI, essentially absent from sera of healthy individuals, was present in those of β-thalassemia patients at levels (1-16 μM) that correlated significantly with those of NTBI measured as mobilizer-dependent chelatable iron or desferrioxamine chelatable iron. Oral treatment of patients with deferiprone (L1) raised plasma NTBI due to iron mobilization but did not lead to LPI appearance, indicating that L1-chelated iron in plasma was not redox active. Moreover, oral L1 treatment eliminated LPI in patients. The approach enabled the assessment of LPI susceptibility to in vivo or in vitro chelation and the potential of LPI to cause tissue damage, as found in iron overload conditions. (Blood. 2003;102:2670-2677)</jats:p> Labile plasma iron in iron overload: redox activity and susceptibility to chelation Blood |
| spellingShingle | Esposito, Breno P., Breuer, William, Sirankapracha, Pornpan, Pootrakul, Pensri, Hershko, Chaim, Cabantchik, Z. Ioav, Blood, Labile plasma iron in iron overload: redox activity and susceptibility to chelation, Cell Biology, Hematology, Immunology, Biochemistry |
| title | Labile plasma iron in iron overload: redox activity and susceptibility to chelation |
| title_full | Labile plasma iron in iron overload: redox activity and susceptibility to chelation |
| title_fullStr | Labile plasma iron in iron overload: redox activity and susceptibility to chelation |
| title_full_unstemmed | Labile plasma iron in iron overload: redox activity and susceptibility to chelation |
| title_short | Labile plasma iron in iron overload: redox activity and susceptibility to chelation |
| title_sort | labile plasma iron in iron overload: redox activity and susceptibility to chelation |
| title_unstemmed | Labile plasma iron in iron overload: redox activity and susceptibility to chelation |
| topic | Cell Biology, Hematology, Immunology, Biochemistry |
| url | http://dx.doi.org/10.1182/blood-2003-03-0807 |