Protective role of selenium against bisphenol-A induced oxidative stress, cytokine generation and apoptosis in SH-SY5Y neuronal cell line

Abstract

Despite the clear effects and harm of the Bisphenol-A (BPH-A) chemical, it is one of the highest produced chemicals worldwide. The main areas of use include building materials, from automotive to food materials. It is important to find therapeutic agents against the damage caused by the BPH-A. Bisphenol A exposure is the major cause of increased oxidative stress (OS) and mitochondrial dysfunction, especially in cells. Thus, our study aimed to research the protective effect of selenium in BPH-A-induced SH-SY5Y neuroblastoma cells. The SH-SY5Y cells were divided into 4 groups as 1- Control group: No drug was applied to these cells. 2- BPH-A group: Bisphenol A was incubated with 100 µM for 24 hours. 3- BPH-A+Na-Se group: This group was incubated with BPH-A for 24 hours. Na-Se (1 µM) was added in the last 2 hours of the 24 hours. 4- Na-Se group: Na-Se was incubated with 1 µM for 2 hours. In the cells, intracellular ROS and JC-1 levels were highest in the BPH-A group, although there was a significant reduction in the selenium-treated group (BPH-A+Na-Se). In addition to these, when the Caspase-3 and Caspase-9 enzyme activities were examined between the groups, it was seen that Selenium reduces the increased caspase activity caused by BPH-A. Finally, when the apoptosis and MTT analysis results between the groups were examined, it was observed that apoptosis and MTT levels were highest in the BPH-A group, while it was significantly lower in the Na-Se group compared to the BPH-A group. In conclusion, this study revealed that Selenium, with its antioxidant properties, can be used as a neuroprotective agent by reducing BPH-A-induced oxidative stress.