Investigation of the Effect of Bisphenol A (BPA) on Ferroptosis in Lung Cancer Cells
6th Life Sciences Congress, Kayseri, Türkiye, 13 - 14 Şubat 2026, ss.47, (Özet Bildiri)
- Yayın Türü: Bildiri / Özet Bildiri
- Basıldığı Şehir: Kayseri
- Basıldığı Ülke: Türkiye
- Sayfa Sayıları: ss.47
- Erciyes Üniversitesi Adresli: Evet
Özet
Bisphenol A (BPA), which is widely used as a key component in the production of industrial polycarbonate plastics and epoxy resins, is a common environmental pollutant present in a broad range of products from food packaging to medical devices, and exposure may also occur via inhalation. Although the endocrine disrupting properties of this compound have been extensively documented in the literature, its toxic effects on lung tissue and the underlying programmed cell death mechanisms remain a current topic of research. While BPA has been reported to induce cell death through apoptosis, necrosis, or autophagy, whether it can trigger cell death via ferroptosis remains unclear. In this study, the effects of Bisphenol A (BPA) exposure on ferroptosis, an iron-dependent form of regulated cell death, were investigated using the human lung adenocarcinoma cell line A549. Within the experimental design, A549 cells were treated with a fixed dose of BPA for 48 hours and harvested at the end of the incubation period. In the initial stage of the molecular analyses, total RNA was isolated from BPA-treated and control A549 cells. Following the assessment of RNA purity and concentration, cDNA synthesis was performed using reverse transcriptase for subsequent gene expression analyses. The primary focus of the study was the expression levels of the GPX4 (Glutathione Peroxidase 4) gene, a key enzyme that protects cells against lipid peroxidation during the ferroptosis process. Changes in GPX4 gene expression were quantitatively analyzed by real-time PCR (qPCR) using the synthesized cDNA samples. The results demonstrated that 48-hour BPA exposure led to a significant reduction of approximately 80% in GPX4 gene expression in A549 cells compared with the control group. This pronounced decrease in GPX4 levels indicates that BPA markedly weakens cellular antioxidant defense mechanisms, thereby rendering cells more susceptible to oxidative damage and ferroptosis.