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1 August 2005 Intracellular Sequestration of 223Ra by the Iron-Storage Protein Ferritin
Michael J. Atkinson, Marianne T. Spanner, Michael Rosemann, Utz Linzner, Walter A. Müller, Wolfgang Gössner
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Abstract

Atkinson, M. J., Spanner, M. T., Rosemann, M., Linzner, U., Müller, W. A. and Gössner, W. Intracellular Sequestration of 223Ra by the Iron-Storage Protein Ferritin. Radiat. Res. 164, 230–233 (2005).

Incorporation of bone-seeking, α-particle-emitting, heavy-metal radionuclides dramatically increases the incidence of osteosarcoma in humans and experimental animals. The accumulation of these radionuclides within the mineral phase of the bone matrix is believed to result in local irradiation of only those proliferating cells close to the bone surface. We now present evidence for a more general pathway for the irradiation of target cells, mediated through the sequestration of heavy-metal radionuclides by the intracellular iron-storage protein ferritin. In vitro studies reveal the transfer of radionuclide from a 223Ra-transferrin complex into immunoprecipitable cytosolic ferritin. In vivo studies confirm the co-localization of incorporated 224Ra and cellular iron stores. This pathway would result in the highly localized irradiation of ferritin-containing cells. Since osteoblastic cells express large quantities of a ferritin isoform specialized in long-term metal storage, we suggest that this may represent an unrecognized source of intracellular irradiation by α-particle-emitting radionuclides. Such a local concentration within target cells has implications both for cellular dosimetry and for inferences of track length and target cell populations within the skeleton.

Michael J. Atkinson, Marianne T. Spanner, Michael Rosemann, Utz Linzner, Walter A. Müller, and Wolfgang Gössner "Intracellular Sequestration of 223Ra by the Iron-Storage Protein Ferritin," Radiation Research 164(2), 230-233, (1 August 2005). https://doi.org/10.1667/RR3410
Received: 11 October 2004; Accepted: 1 March 2005; Published: 1 August 2005
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