Meeting Abstract
When produced in excess, reactive oxygen species (ROS) can cause damage that has lasting impacts on cellular performance. However, when cells are exposed to modest levels of ROS, the cells upregulate signaling processes that improve cellular performance. In a prior study, we induced ROS emission in mice via X-irradiation and found that 24 hours post exposure, ROS production and oxidative damage increased, but 10 days after X-irradiation exposure both ROS production and oxidative damage levels fell to below non-irradiated control levels. This finding suggests that despite initial damage, cells may experience improved condition following a modest oxidative event. The aim of the current study is to deduce the mechanisms responsible for this hormetic effect. We employed a cell culture model, and our goal was to determine if AML12 mouse hepatocytes display a response to ROS that is comparable to liver cells of mice exposed to X-irradiation. Mitochondrial function and ROS emission of hepatocytes were measured 1, 24, 48, and 72 hours after X-irradiation. The levels of oxidative damage, antioxidants, and select transcriptional factors that are targets of ROS signaling, including Nrf-2, PCG-1α , and PPAR-γ were measured. Results for radiated cells and non-irradiated control cells will be described. Future studies will identify the pathways response for the hormetic effect by up- and down-regulating identified candidate genes.
