Bone as Target Organ for Metals: The Case of f-Elements

Vidaud, Claude; Bourgeois, Damien; Meyer, Daniel

doi:10.1021/tx300064m

Cited by 113 publications

(75 citation statements)

References 156 publications

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“…Adsorption of trace elements onto bone in vivo increases relative to other body pools in the order U, light REE (LREE: La, Ce, Nd), middle REE (MREE: Eu, Gd), and Th plus heavy REE (HREE: Yb, Lu; see review of ref. 17; Fig. S1).…”

Section: Discussionmentioning

confidence: 99%

Trace element diffusivities in bone rule out simple diffusive uptake during fossilization but explain in vivo uptake and release

Kohn

Moses

2012

Proc. Natl. Acad. Sci. U.S.A.

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Diffusion rates of numerous trace elements in bone at 20°C were determined using laser-ablation inductively coupled plasma mass spectrometry analysis of experimentally induced diffusion profiles. Diffusivities are about 1 order of magnitude slower than current semiquantitative geochemical views and about 1.5 orders of magnitude faster than indirect radiotracer estimates. Intrabone volume diffusion is too slow and too similar among many elements to explain trace element profiles in young fossils and archeological materials. Diffusivity differences among elements do, however, explain disparate biokinetic washout of Sr vs. Ba and of light vs. heavy rare earth elements (REEs). These results improve the understanding of the physical principles underlying biokinetic models and rates and mechanisms of trace element alteration of phosphatic tissues in paleontological, archeological, and crystal-chemical contexts. Recrystallization and transport limitations in soils explain trace element profiles in young fossils better than intrabone volume diffusion alone and imply that diffusion of REE and other trivalent cations is likely controlled by a common charge-compensating species rather than ionic radii or partition coefficients.T race elements can pose major health risks, especially radioactive products of nuclear processes. Many of these elements concentrate in bone (bone-seeking elements), including P, Ca, Zn, Sr, Ba, lanthanides, Pb, and actinides, where they can reside for decades before being gradually eliminated from the body (1). Bone's tenacious affinity for certain trace elements persists postmortem, as evidenced by orders of magnitude higher concentrations of trace elements in archeological bones and fossils compared with modern tissues (2). The question of how the bone mineral bioapatite-a calcium phosphate-takes up and releases these elements has launched a lively debate among numerous research groups. Health physicists have long debated in vivo remodeling (biologically controlled resorption and reprecipitation of bioapatite) vs. volume diffusion for explaining the slowest rates of uptake and release (3-8); such research is commonly termed biokinetics. Geochemists debate in vitro recrystallization and surface adsorption vs. diffusion for explaining trace element profiles in fossils, although diffusive processes are normally assumed (9, 10). Diffusion underpins both types of research because it provides a strict lower limit for rates of trace element uptake and release both in vivo and in vitro. Understanding diffusion rates therefore improves predictions of long-term clearance of trace elements from the body, as well as geological or archeological interpretations of trace elements or their isotopes, such as U-series geochronology, conditions of deposition and fossilization, and forensic discrimination among fossils (2).Surprisingly, virtually no experiments constrain trace element diffusion rates in bone, and we can find no studies that measured diffusion profiles directly. Consequently, we conducted 18-mo exper...

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Section: Discussionmentioning

confidence: 99%

Trace element diffusivities in bone rule out simple diffusive uptake during fossilization but explain in vivo uptake and release

Kohn

Moses

2012

Proc. Natl. Acad. Sci. U.S.A.

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“…52 Molecular levels studies are clearly needed to identify common modes of action and the biochemical effects of REEs. Future research should evaluate REE concentrations in internal organs and/or whole organism concentrations (including bones) because muscle concentrations may not provide accurate estimates of REE exposure.…”

Section: Tissue-specific Ree Bioaccumulationmentioning

confidence: 99%

Rare earth elements (REE) in freshwater, marine, and terrestrial ecosystems in the eastern Canadian Arctic

MacMillan

Chételat

Heath

et al. 2017

Preprint

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Few ecotoxicological studies exist for rare earth elements (REEs), particularly fieldbased studies on their bioaccumulation and food web dynamics. REE mining has led to significant environment impacts in several countries (China, Brazil, U.S.), yet little is known about the fate and transport of these contaminants of emerging concern. To understand how REEs behave in pristine northern food webs, we measured REE concentrations and carbon and nitrogen stable isotope ratios (∂ 15 N, ∂ 13 C) in biota from marine, freshwater, and terrestrial ecosystems of the eastern Canadian Arctic (N=339). Northern ecosystems are potentially vulnerable to REE enrichment from prospective mining projects at high latitudes. Wildlife harvesting and tissue sampling was partly conducted by local hunters through a communitybased monitoring project. Results show that REE generally follow a coherent bioaccumulation pattern for sample tissues, with some anomalies for redox-sensitive elements (Ce, Eu). Highest REE concentrations were found at low trophic levels, especially in vegetation and aquatic invertebrates. Terrestrial herbivores, ringed seal, and fish had low REE levels in muscle tissue (<0.1 nmolg -1 ), yet accumulation was an order of magnitude higher in all liver tissues. Age-and length-dependent REE accumulation also suggest that REE uptake is faster than elimination for some species. Overall, REE bioaccumulation patterns appear to be species-and tissue-species, with limited potential for biomagnification. This study provides novel ecotoxicological data on the behaviour of REE in ecosystems and will be useful for environmental impact assessment of REE enrichment in northern regions.peer-reviewed)

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“…The tissue distribution of an actinide will therefore determine the pattern of injury observed and its radiological and chemical toxicities may lead to serious adverse health effects (6)(7)(8). Although they are known to rapidly circulate and deposit into major organs such as bone, liver, or kidney after contamination (6,(8)(9)(10), the specific molecular mechanisms associated with mammalian uptake of these toxic heavy elements remain largely unexplored. Proposed mammalian actinide acquisition and transport mechanisms have typically focused on proteins that use conserved motifs to directly bind the essential elements iron or calcium (6,8,(10)(11)(12)(13), such as transferrin (14)(15)(16)(17)(18), ferritin (13), osteopontin (19), or fetuin (20).…”

mentioning

confidence: 99%

“…Although they are known to rapidly circulate and deposit into major organs such as bone, liver, or kidney after contamination (6,(8)(9)(10), the specific molecular mechanisms associated with mammalian uptake of these toxic heavy elements remain largely unexplored. Proposed mammalian actinide acquisition and transport mechanisms have typically focused on proteins that use conserved motifs to directly bind the essential elements iron or calcium (6,8,(10)(11)(12)(13), such as transferrin (14)(15)(16)(17)(18), ferritin (13), osteopontin (19), or fetuin (20). Siderocalin (Scn), an essential antibacterial protein that sequesters iron (21,22), and an important component of iron trafficking (23), is distinct in that it binds ferric iron indirectly, through tight complexes with a siderophore or siderophore-derived chelator.…”

mentioning

confidence: 99%

Siderocalin-mediated recognition, sensitization, and cellular uptake of actinides

Allred

Rupert

Gauny

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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Synthetic radionuclides, such as the transuranic actinides plutonium, americium, and curium, present severe health threats as contaminants, and understanding the scope of the biochemical interactions involved in actinide transport is instrumental in managing human contamination. Here we show that siderocalin, a mammalian siderophore-binding protein from the lipocalin family, specifically binds lanthanide and actinide complexes through molecular recognition of the ligands chelating the metal ions. Using crystallography, we structurally characterized the resulting siderocalin-transuranic actinide complexes, providing unprecedented insights into the biological coordination of heavy radioelements. In controlled in vitro assays, we found that intracellular plutonium uptake can occur through siderocalin-mediated endocytosis. We also demonstrated that siderocalin can act as a synergistic antenna to sensitize the luminescence of trivalent lanthanide and actinide ions in ternary protein-ligand complexes, dramatically increasing the brightness and efficiency of intramolecular energy transfer processes that give rise to metal luminescence. Our results identify siderocalin as a potential player in the biological trafficking of f elements, but through a secondary ligandbased metal sequestration mechanism. Beyond elucidating contamination pathways, this work is a starting point for the design of twostage biomimetic platforms for photoluminescence, separation, and transport applications.actinide transport | siderocalin | protein crystallography | luminescence spectroscopy | antenna effect E vents of the last decade have heightened public concern that radionuclides may be released to the environment either deliberately or accidentally (1, 2), with such events potentially leading to the internal contamination of a large number of individuals. The actinides are all highly radioactive, as are some lanthanide fission products, and many of their isotopes decay by alpha particle emission (3). Once internalized, they are distributed to various tissues with patterns that depend on the chemical and physical form of the contaminant in question (4). The densely ionizing alpha particles emitted by actinides when retained can cause tissue damage and induce cancer in target tissues in a dosedependent manner (5). Sufficiently high radionuclide doses may also cause manifestations of acute radiation syndrome. The tissue distribution of an actinide will therefore determine the pattern of injury observed and its radiological and chemical toxicities may lead to serious adverse health effects (6-8). Although they are known to rapidly circulate and deposit into major organs such as bone, liver, or kidney after contamination (6,(8)(9)(10), the specific molecular mechanisms associated with mammalian uptake of these toxic heavy elements remain largely unexplored. Proposed mammalian actinide acquisition and transport mechanisms have typically focused on proteins that use conserved motifs to directly bind the essential elements iron or calcium (6, 8, 10-...

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Bone as Target Organ for Metals: The Case of f-Elements

Cited by 113 publications

References 156 publications

Trace element diffusivities in bone rule out simple diffusive uptake during fossilization but explain in vivo uptake and release

Trace element diffusivities in bone rule out simple diffusive uptake during fossilization but explain in vivo uptake and release

Rare earth elements (REE) in freshwater, marine, and terrestrial ecosystems in the eastern Canadian Arctic

Siderocalin-mediated recognition, sensitization, and cellular uptake of actinides

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