Induction of reactive oxygen species and apoptosis in BEAS-2B cells by mercuric chloride.

Abstract

Mercury is a widespread environmental and industrial pollutant that induces serious adverse effects in both humans and the environment. However, the toxicities and its mechanisms have not been fully elucidated. Among the proposed mechanisms of biological toxicities, the intracellular level of thiol group (-SH) and oxidative stress have been widely studied. In this study, production of reactive oxygen species (ROS) by mercuric chloride (2, 4, 6, and 8 ppm as of mercury) was investigated in cultured human bronchial epithelial cells (BEAS-2B cell line). Exposure of cultured cells to mercuric chloride led to cell death, ROS increase, and cytosolic caspase-3 activation. The ROS increase was related to the decreased level of GSH. Chromatin condensation evaluated by 4',6-diamidino-2-phenylindole (DAPI) staining were also shown in mercury-treated cells and this suggest the apoptotic process of cells by mercuric chloride.