Abstract: SA-PO927
Microplastics and Bisphenol A Coexposure on Human Kidney Proximal Tubular Cells
Session Information
- Pathology and Lab Medicine - 2
October 26, 2024 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Pathology and Lab Medicine
- 1800 Pathology and Lab Medicine
Authors
- Estienne, Luca, Azienda Ospedaliera Nazionale Santi Antonio e Biagio e Cesare Arrigo Alessandria, Alessandria, Piemonte, Italy
- Verzola, Daniela, IRCCS Ospedale Policlinico San Martino, Genova, Italy
- Esposito, Pasquale, IRCCS Ospedale Policlinico San Martino, Genova, Italy
- Viazzi, Francesca, IRCCS Ospedale Policlinico San Martino, Genova, Italy
- Angeletti, Andrea, Istituto Giannina Gaslini, Genova, Liguria, Italy
- Cravedi, Paolo, Icahn School of Medicine at Mount Sinai, New York, New York, United States
- Quaglia, Marco, Azienda Ospedaliera Nazionale Santi Antonio e Biagio e Cesare Arrigo Alessandria, Alessandria, Piemonte, Italy
- La Porta, Edoardo, Istituto Giannina Gaslini, Genova, Liguria, Italy
Background
Microplastics (MPs) accumulate in human tissues, including kidney. Beyond direct harmful actions, MPs can also adsorb a wide range of toxic substances, such as Bisphenol A (BPA) and so, enhancing their toxicity. MPs have been found in human blood, urine, and several human tissues, including lungs, placenta, blood, heart, and the kidney by Massardo et al. Moreover, it have recently demonstrated that patients with evidence of MPs in carotid artery plaque experience an increased risk of death and cardiovascular event compared with those without MPs .
Methods
We exposed a proximal tubular cell line for 5-24 hours to polyethylene (PE)-MPs and BPA alone or combined. MP characterization was performed by by means of Dynamic Light Scattering analyses. We analyzed molecules involved in renal damage through mRNA Analysis, Immunofluorescence and immunocytochemistry and Western Blot Analysis
Results
Compared with the single exposure, the co-treatment was more powerful, reducing cell viability and boosting the pro-oxidant a pro-inflammatory response. Exposition to co-treatment induced a 3.5 and 2.7 fold increase of CCL-2 and -5 (both p<0.05 vs CTR). In addition, Heat Shock protein (HSP90), a chaperone involved in multiple cellular functions, was reduced, while Aryl hydrocarbon receptor (AHR) expression, a transcription factor which binds multiple environmental ligands, was increased.
Conclusion
Our study demonstrates that all the treatments influenced the cell behavior, but the co-exposure was more incisive. The combination of PE-MPs and BPA can negatively modify the cellular homeostasis, contributing to the induction of kidney damage.