Bisphenol A (BPA) is an organic compound that is widely used in plastic products. It acts as an endocrine disruptor capable of mimicking or modifying the activity of endogenous hormones. Recent data have shown that exposure to BPA increases the risk of type 2 diabetes. The aim of this study was to examine the effects of BPA on beta-TC-6 mice cells. Cells were incubated with serial dilutions of BPA: control group, 0.002μM, 0.02μM, 0.1μM, and 0.2μM for 12, 24, 48 and 72 hours. Cell viability and proliferation levels were determined by measuring intracellular ATP levels. BPA effects on beta-TC-6 cells were investigated by studying gene expression regulated at the transcriptional RNA level by real time PCR technique (citrate synthase and ATP synthase 6) and protein concentrations regulated at the translational levels by western blot analysis. The aging rate of cells was studied using SenTraGor TM. Exposure of beta-TC-6 cells to all BPA concentrations resulted in significant decreases of intracellular ATP levels when compared with the control group (all p<0.05). Moreover, exposure of beta-TC-6 cells to 0,2μM BPA concentration for 24 and 48 hours resulted in significant increases in the relative gene expression levels and in increased expression of proteins involved in apoptosis. The percentage of aging cells was >20% of total number of cells 24 hours after incubation at the 2 higher concentrations of BPA and was significantly increased when compared with the control group and the lower concentration of BPA. BPA affects viability, function and aging of beta-TC-6 cells. BPA presumably increases apoptosis rate and induces mitochondrial dysfunction on beta-TC-6 cells in a dose-dependent manner.


I. Anastasiou: None. I. Eleftheriadou: None. A. Tentolouris: None. A. Angelopoulou: None. O. Kosta: None. I. Mourouzis: None. N. Tentolouris: None.

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