Abstract
Natural uranium exhibits chemical toxicity, especially known with its acute effects on kidney. Simultaneously, it has been proved that uranium accumulates in bones during long-term exposure[1] but its chronical effects on bones are not clear. Particularly the mechanisms associated to accumulation into and release from bones are unknown, which is key to design and test decorporation reagents in future. Bone is a complicated organ, composed of mineralized apatite and organic compounds (mostly type I collagen). Our work is dedicated to the understanding of how uranium is accumulated in the inorganic bone matrix through chemical pathways, and what factors influence the solid/liquid equilibrium between uranium and the bone. To fulfil this goal, apatite materials which mimic bone apatite have been synthesized, with and without uranium. Such apatite materials have been pre-equilibrated with a fluid mimicking blood plasma at physiological pH=7.4.
Highlights
The proposed exchange mechanism of +2 cations (Ca2+, Zn2+, etc.) with bone relies on a two compartment model[2], including ion exchange in the amorphous hydration shell and further ion diffusion into the mineral matrix
It has been proved that uranium accumulates in bones during longterm exposure[1] but its chronical effects on bones are not clear
Our work is dedicated to the understanding of how uranium is accumulated in the inorganic bone matrix through chemical pathways, and what factors influence the solid/liquid equilibrium between uranium and the bone
Summary
The proposed exchange mechanism of +2 cations (Ca2+, Zn2+, etc.) with bone relies on a two compartment model[2], including ion exchange in the amorphous hydration shell and further ion diffusion into the mineral matrix. Natural uranium exhibits chemical toxicity, especially known with its acute effects on kidney. It has been proved that uranium accumulates in bones during longterm exposure[1] but its chronical effects on bones are not clear.
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