The effect of boric acid administration on glutathione peroxidase enzyme activity in hepatocellular carcinoma (HEPG2 cell line)

The effect of boric acid administration on glutathione peroxidase enzyme activity in hepatocellular carcinoma (HepG2 cell line) Hepatocellular carcinoma is the most common form of primary liver malignancy and usually occurs in patients with chronic liver disease and cirrhosis. Cytochrome P450 (CYP450); is an enzyme system involved in the synthesis of drugs, xenobiotics, cholesterol, bile acid, and steroids and their degradation. It is known that the increased activity of CYP450 enzyme leads to lipid peroxidation and the formation of ROS. The enzyme glutathione peroxidase (GPx) is an antioxidant enzyme located in the cytoplasm of cells that protects cells from oxidative damage by H2O2. GPx enzyme has been shown to inhibit angiogenesis and proliferation of tumor cells and prevent the development of hepatocellular carcinoma and suppress its progression through immune-mediated mechanisms. Inhibition of the GPx enzyme leads to programmed death of the cell. The element boron is absorbed into the body with drinking water and plant foods, it is almost completely absorbed in the liver. It circulates in the blood as boric acid and it induces apoptosis in some types of cancer. In this study, the effect of boric acid on glutathione peroxidase enzyme activity was investigated in the HepG2 cell line. The GPx enzyme cells were measured spectrophotometrically. Boric acid was found to have an inhibitory effect on the GPx enzyme. According to these results, the inhibition levels were measured by applying the cell viability assay to determine the cytotoxicity of boric acid on the GPx enzyme. In this study, the boric acid dose to be applied to HepG2 cells was set at 236.7 mM using the GraphPad Prism 9 program. In addition, the significance levels of GPx concentrations in HepG2 cells with and without boric acid application were again determined using the GraphPad Prism 9 program. As a result, boric acid showed a significant inhibitory effect on HepG2 cells at the level of glutathione peroxidase enzyme activity. Keywords: Boric Acid, Glutathione Peroxidase, Hepatocellular Carcinoma