Back
For best output, select "Paper Size" as "A4" and "Margin" as "0" or "None".
To save or print to PDF, please select Print Destination > Save as PDF, enable Background Graphics under "More Settings", then click "Save".
During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Over the past century, large quantities of plastics have been produced, utilized and disposed into the environment where, under solar UV irradiation, the structure and properties of plastics undergo inevitable changes. To date, microplastics (MPs) have been detected in many human organs, including the kidney, and in several experimental models, detrimental effects of virgin (V) MPs have been shown, but little is known about the action of photoaged MPs on renal cells. The aims of our study are to evaluate the effects of V and oxidized (OX) MPs on human proximal renal tubular cell (HK-2) phenotype. To this end, genotoxic damage, p57 (a cell-cycle inhibitor), and cytoskeletal alterations (γ-tubulin, F-actin polymerization) were explored.
To induce UVB aging, polystyrene MPs (1 μm) were oxidized under UVB lamp exposure (318 nm) in the presence of 40% hydrogen peroxide for 96 hours. HK-2 cells were exposed to 0 (CTR), 25, and 50 μg/mL virgin (V) or oxidized (OX) MPs for 48 hours. Comet assay was performed to evaluate genotoxic damage and expressed as percentage of DNA in the tail. γ-tubulin and p57 expression were analyzed by Western blot and by RT-PCR. By confocal microscopy, the amount of F-actin was evaluated in phalloidin-stained cells.
In cells treated with MPs, Comet assay showed a significant increase in %Tail DNA with respect to CTR (1.5–5 fold vs. CTR; p < 0.05–0.001), particularly in OX-MP–treated cells. p57 protein and mRNA levels were increased by all treatments, especially by 50 μg/mL V and OX MPs (p < 0.05–0.006 vs. CTR). Both V and OX MPs decreased γ-tubulin expression (−20–50% vs. CTR, p < 0.05). On the other hand, phalloidin staining revealed a compact polymerization of F-actin in stress fibers along the major cell axis in CTR and V-exposed cells, but this was absent in OX treatments.
Our study shows that in HK-2, MPs, also following natural degradation and oxidation processes, can cause genotoxic stress, cell-cycle arrest, and cytoskeletal disruption which could contribute to pathogenesis of kidney disease. Interestingly, oxidized MPs, that reflect more real-life MPs exposure, caused stronger effects, suggesting environmental degradation of MPs could increase kidney toxicity. These results underscore the importance of using more realistic test materials when investigating kidney health risk secondary to MPs exposure.
