Non-transferrin bound iron: A key role in iron overload and iron toxicity
Besides transferrin iron, which represents the normal form of circulating iron, non-transferrin bound iron (NTBI) has been identified in the plasma of patients with various pathological conditions in which transferrin saturation is significantly elevated. To show that: i) NTBI is present not only du...
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| Published in | Biochimica et biophysica acta Vol. 1820; no. 3; pp. 403 - 410 |
|---|---|
| Main Authors | , , , |
| Format | Journal Article |
| Language | English |
| Published |
Netherlands
Elsevier B.V
01.03.2012
Elsevier |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0304-4165 0006-3002 1872-8006 |
| DOI | 10.1016/j.bbagen.2011.07.014 |
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| Abstract | Besides transferrin iron, which represents the normal form of circulating iron, non-transferrin bound iron (NTBI) has been identified in the plasma of patients with various pathological conditions in which transferrin saturation is significantly elevated.
To show that: i) NTBI is present not only during chronic iron overload disorders (hemochromatosis, transfusional iron overload) but also in miscellaneous diseases which are not primarily iron overloaded conditions; ii) this iron species represents a potentially toxic iron form due to its high propensity to induce reactive oxygen species and is responsible for cellular damage not only at the plasma membrane level but also towards different intracellular organelles; iii) the NTBI concept may be expanded to include intracytosolic iron forms which are not linked to ferritin, the major storage protein which exerts, at the cellular level, the same type of protective effect towards the intracellular environment as transferrin in the plasma.
Plasma NTBI and especially labile plasma iron determinations represent a new important biological tool since elimination of this toxic iron species is a major therapeutic goal.
The NTBI approach represents an important mechanistic concept for explaining cellular iron excess and toxicity and provides new important biochemical diagnostic tools. This article is part of a Special Issue entitled Transferrins: Molecular mechanisms of iron transport and disorders.
► NTBI and its toxic form LPI appear in plasma when transferrin saturation increases. ► NTBI is avidly taken up by parenchymal cells (especially hepatocytes). ► Labile Iron Pool can be considered as an intracytosolic equivalent of plasma NTBI. ► NTBI can be present in diseases not primarily related to iron overload. ► Therapeutic efforts (phlebotomies, iron chelation) must focus on NTBI elimination. |
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| AbstractList | BACKGROUND: Besides transferrin iron, which represents the normal form of circulating iron, non-transferrin bound iron (NTBI) has been identified in the plasma of patients with various pathological conditions in which transferrin saturation is significantly elevated. SCOPE OF THE REVIEW: To show that: i) NTBI is present not only during chronic iron overload disorders (hemochromatosis, transfusional iron overload) but also in miscellaneous diseases which are not primarily iron overloaded conditions; ii) this iron species represents a potentially toxic iron form due to its high propensity to induce reactive oxygen species and is responsible for cellular damage not only at the plasma membrane level but also towards different intracellular organelles; iii) the NTBI concept may be expanded to include intracytosolic iron forms which are not linked to ferritin, the major storage protein which exerts, at the cellular level, the same type of protective effect towards the intracellular environment as transferrin in the plasma. MAJOR CONCLUSIONS: Plasma NTBI and especially labile plasma iron determinations represent a new important biological tool since elimination of this toxic iron species is a major therapeutic goal. GENERAL SIGNIFICANCE: The NTBI approach represents an important mechanistic concept for explaining cellular iron excess and toxicity and provides new important biochemical diagnostic tools. This article is part of a Special Issue entitled Transferrins: Molecular mechanisms of iron transport and disorders. Besides transferrin iron, which represents the normal form of circulating iron, non-transferrin bound iron (NTBI) has been identified in the plasma of patients with various pathological conditions in which transferrin saturation is significantly elevated. To show that: i) NTBI is present not only during chronic iron overload disorders (hemochromatosis, transfusional iron overload) but also in miscellaneous diseases which are not primarily iron overloaded conditions; ii) this iron species represents a potentially toxic iron form due to its high propensity to induce reactive oxygen species and is responsible for cellular damage not only at the plasma membrane level but also towards different intracellular organelles; iii) the NTBI concept may be expanded to include intracytosolic iron forms which are not linked to ferritin, the major storage protein which exerts, at the cellular level, the same type of protective effect towards the intracellular environment as transferrin in the plasma. Plasma NTBI and especially labile plasma iron determinations represent a new important biological tool since elimination of this toxic iron species is a major therapeutic goal. The NTBI approach represents an important mechanistic concept for explaining cellular iron excess and toxicity and provides new important biochemical diagnostic tools. This article is part of a Special Issue entitled Transferrins: Molecular mechanisms of iron transport and disorders. Besides transferrin iron, which represents the normal form of circulating iron, non-transferrin bound iron (NTBI) has been identified in the plasma of patients with various pathological conditions in which transferrin saturation is significantly elevated.BACKGROUNDBesides transferrin iron, which represents the normal form of circulating iron, non-transferrin bound iron (NTBI) has been identified in the plasma of patients with various pathological conditions in which transferrin saturation is significantly elevated.To show that: i) NTBI is present not only during chronic iron overload disorders (hemochromatosis, transfusional iron overload) but also in miscellaneous diseases which are not primarily iron overloaded conditions; ii) this iron species represents a potentially toxic iron form due to its high propensity to induce reactive oxygen species and is responsible for cellular damage not only at the plasma membrane level but also towards different intracellular organelles; iii) the NTBI concept may be expanded to include intracytosolic iron forms which are not linked to ferritin, the major storage protein which exerts, at the cellular level, the same type of protective effect towards the intracellular environment as transferrin in the plasma.SCOPE OF THE REVIEWTo show that: i) NTBI is present not only during chronic iron overload disorders (hemochromatosis, transfusional iron overload) but also in miscellaneous diseases which are not primarily iron overloaded conditions; ii) this iron species represents a potentially toxic iron form due to its high propensity to induce reactive oxygen species and is responsible for cellular damage not only at the plasma membrane level but also towards different intracellular organelles; iii) the NTBI concept may be expanded to include intracytosolic iron forms which are not linked to ferritin, the major storage protein which exerts, at the cellular level, the same type of protective effect towards the intracellular environment as transferrin in the plasma.Plasma NTBI and especially labile plasma iron determinations represent a new important biological tool since elimination of this toxic iron species is a major therapeutic goal.MAJOR CONCLUSIONSPlasma NTBI and especially labile plasma iron determinations represent a new important biological tool since elimination of this toxic iron species is a major therapeutic goal.The NTBI approach represents an important mechanistic concept for explaining cellular iron excess and toxicity and provides new important biochemical diagnostic tools. This article is part of a Special Issue entitled Transferrins: Molecular mechanisms of iron transport and disorders.GENERAL SIGNIFICANCEThe NTBI approach represents an important mechanistic concept for explaining cellular iron excess and toxicity and provides new important biochemical diagnostic tools. This article is part of a Special Issue entitled Transferrins: Molecular mechanisms of iron transport and disorders. Besides transferrin iron, which represents the normal form of circulating iron, non-transferrin bound iron (NTBI) has been identified in the plasma of patients with various pathological conditions in which transferrin saturation is significantly elevated. To show that: i) NTBI is present not only during chronic iron overload disorders (hemochromatosis, transfusional iron overload) but also in miscellaneous diseases which are not primarily iron overloaded conditions; ii) this iron species represents a potentially toxic iron form due to its high propensity to induce reactive oxygen species and is responsible for cellular damage not only at the plasma membrane level but also towards different intracellular organelles; iii) the NTBI concept may be expanded to include intracytosolic iron forms which are not linked to ferritin, the major storage protein which exerts, at the cellular level, the same type of protective effect towards the intracellular environment as transferrin in the plasma. Plasma NTBI and especially labile plasma iron determinations represent a new important biological tool since elimination of this toxic iron species is a major therapeutic goal. The NTBI approach represents an important mechanistic concept for explaining cellular iron excess and toxicity and provides new important biochemical diagnostic tools. This article is part of a Special Issue entitled Transferrins: Molecular mechanisms of iron transport and disorders. ► NTBI and its toxic form LPI appear in plasma when transferrin saturation increases. ► NTBI is avidly taken up by parenchymal cells (especially hepatocytes). ► Labile Iron Pool can be considered as an intracytosolic equivalent of plasma NTBI. ► NTBI can be present in diseases not primarily related to iron overload. ► Therapeutic efforts (phlebotomies, iron chelation) must focus on NTBI elimination. |
| Author | Loréal, Olivier Brissot, Pierre Ropert, Martine Le Lan, Caroline |
| Author_xml | – sequence: 1 givenname: Pierre surname: Brissot fullname: Brissot, Pierre email: pierre.brissot@univ-rennes1.fr organization: Inserm, UMR991, Liver Metabolisms and Cancer, F-35033 Rennes, France – sequence: 2 givenname: Martine surname: Ropert fullname: Ropert, Martine organization: Inserm, UMR991, Liver Metabolisms and Cancer, F-35033 Rennes, France – sequence: 3 givenname: Caroline surname: Le Lan fullname: Le Lan, Caroline organization: Inserm, UMR991, Liver Metabolisms and Cancer, F-35033 Rennes, France – sequence: 4 givenname: Olivier surname: Loréal fullname: Loréal, Olivier organization: Inserm, UMR991, Liver Metabolisms and Cancer, F-35033 Rennes, France |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/21855608$$D View this record in MEDLINE/PubMed https://hal.science/hal-00739430$$DView record in HAL |
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| Snippet | Besides transferrin iron, which represents the normal form of circulating iron, non-transferrin bound iron (NTBI) has been identified in the plasma of patients... BACKGROUND: Besides transferrin iron, which represents the normal form of circulating iron, non-transferrin bound iron (NTBI) has been identified in the plasma... |
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| SubjectTerms | Cell Death ferritin Ferritins - blood Ferroportin Hemochromatosis Hemochromatosis - blood Hepcidin Human health and pathology Humans Hépatology and Gastroenterology Ion Transport iron Iron - blood Iron - metabolism Iron overload Iron Overload - blood Life Sciences Liver - metabolism Non-transferrin bound iron (NTBI) organelles patients plasma membrane reactive oxygen species Reactive Oxygen Species - metabolism Thalassemia toxicity transferrin Transferrin - metabolism |
| Title | Non-transferrin bound iron: A key role in iron overload and iron toxicity |
| URI | https://dx.doi.org/10.1016/j.bbagen.2011.07.014 https://www.ncbi.nlm.nih.gov/pubmed/21855608 https://www.proquest.com/docview/2000010382 https://www.proquest.com/docview/922758654 https://hal.science/hal-00739430 |
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