Bisphenol A-induced apoptosis, oxidative stress and DNA damage in cultured rhesus monkey embryo renal epithelial Marc-145 cells

Abstract

Bisphenol A (BPA) is widely used in the production of epoxy resins and polycarbonate plastics. Under harsh situations, these plastics likely desorb BPA, which then can seep into the environment. Various concentrations of BPA have been detected in most biological fluid. However, there is paucity of information on the detrimental effects of BPA and its subsequent cellular events in chronic kidney disease (CKD). Hence, in this in vitro study, we aimed to investigate the effects of BPA on renal epithelial cell activation, apoptosis, and DNA damage. Rhesus monkey embryo renal epithelial Marc-145 cells were exposed to 0, 10−1, 10−2, 10−3, 10−4, 10−5, and 10−6 M of BPA. Alterations in intracellular apoptosis, oxidative stress, and DNA damage were evaluated. The results showed that BPA decreased cell viability, superoxide dismutase (SOD) activity and glutathione (GSH) level, with concomitant increases in apoptosis related indices, lactate dehydrogenase (LDH) activity, reactive oxygen species (ROS) generation, thiobarbituric acid reactive substances (TBARS) content, and the rate of comet Marc-145 cells with a dose-dependent manner. The data indicated that increased oxidative stress, apoptosis and DNA damage in epithelial Marc-145 cells might play a pivotal role in the mechanism of BPA-induced nephrotoxicity.