부산대학교 도서관

R2881 --> Background: Bisphenol‐A (BPA) is a synthetic chemical used in the production of polycarbonate plastics and epoxy resins. It can be found ubiquitously in consumer and medical products, such as food containers, water pipes, dental sealants, and electronics. Human exposure to BPA is widespread, and the chemical has been detected in 93% of urinary samples from the U.S. Additionally, intensive care and cardiac surgery patients are exposed to exceedingly high BPA concentrations through contact with plastic medical devices. This is concerning, given that BPA exposure has been connected with a risk of adverse cardiovascular events. As the health risk of BPA has become apparent, structural analogues are being utilized as replacement chemicals, including BPF and BPS. Despite their continued use, the effects of BPF and BPS on cardiac health are unknown. Objective: This study aimed to quantify the safety and toxicity of BPA exposure on cardiomyocyte electrophysiology, compared to structural analogues BPF and BPS. Hypothesis: We hypothesized that recently developed replacement chemicals, such as BPF and BPS, are safer with less adverse cardiac effects, as compared with BPA. Methods: Cardiomyocytes differentiated from human‐induced pluripotent stem cells (hiPSC‐CMs) were cultured on an Axion Maestro Edge microelectrode array (MEA) system. Cells were treated with bisphenol‐analogues (10 nM ‐ 100 μM) for 5 minutes and electrophysiological parameters were recorded in response to external pacing (1.5 Hz). Results: The field potential duration (FPD) of cultured hiPSC‐CMs demonstrated a dose‐dependent response for BPA. At the lowest dose, 10 nM BPA, no effect was observed. At a 10‐fold higher dose, 100 nM BPA, there was a non‐significant prolongation of FPD compared to the DMSO vehicle control (5.76% increase, p=0.1252). At increasing doses, FPD shortened significantly compared to the DMSO vehicle control (30 μM: 12.33% decrease, p<0.0001 and 100 μM: 39.82% decrease, p=0.0017). No significant low‐dose effects were observed for BPF and BPS. However, treatment with BPF displayed FPD shortening at high doses (30 μM: 13.43% decrease, p<0.0001 and 100 μM: 34.52% decrease, p<0.0001). Conversely, treatment with BPS displayed no significant change in FPD across all tested concentrations. Conclusion: BPF, but not BPS, caused FPD shortening to a similar extent as BPA. These results revealed that replacement products for BPA, such as BPS, may be a safer alternative for medical product materials. [ABSTRACT FROM AUTHOR]