Lead
oxide nanoparticles (PbONPs), upon their entry into the lungs via inhalation, induce structural changes in primary and
secondary target organs. The fate and ultrastructural localization
of PbONPs in organs is known to be dependent on the specific organ.
Here, we focused on the differences in the ability to clear the inhaled
PbONPs from secondary target organs and on molecular and cellular
mechanisms contributing to nanoparticle removal. Mice were exposed
to PbONPs in whole-body inhalation chambers. Clearance of ionic lead
and PbONPs (Pb/PbONPs) from the lungs and liver was very effective,
with the lead being almost completely eliminated from the lungs and
the physiological state of the lung tissue conspicuously restored.
Kidneys exposed to nanoparticles did not exhibit serious signs of
damage; however, LA-ICP-MS uncovered a certain amount of lead located
preferentially in the kidney cortex even after a clearance period.
The concentration of lead in femurs, as representatives of the axial
skeleton, was the highest among studied organs at all designated time
points after PbONP exposure, and the clearance ability of lead from
the femurs was very low in contrast to other organs. The organ-specific
increase of ABC transporters expression (ABCG2 in lungs and ABCC3
in the liver) was observed in exposed animals, suggesting their involvement
in removing Pb/PbONPs from tissues. Moreover, the expression of caveolins and clathrin displayed a tissue-specific
response to lead exposure. Our results uncovered high variability
among the organs in their ability to clear Pb/PbONPs and in the transporters
involved in this process.
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