Meeting Abstract
Reactive oxygen species (ROS) can induce oxidative stress, but ROS also serve as signaling molecules that can lead to improve cellular performance. In a prior study, we characterized the temporal response to induced ROS production via X-irradiation in mice. Our results show that liver mitochondrial damage increased 24 h post exposure, but the liver displayed improved markers of mitochondrial function 10 days after X-irradiation. This adaptive response is referred to as mitohormesis. To identify the mechanisms associated with this effect, we asked if AML12 (mouse) hepatocytes displayed a response to radiation that was similar to our previous study. We evaluated temporal changes in the cells following 25 cGy of X-irradiation by measuring mitochondrial function and ROS emission 1, 24, 48, and 72 h after X-irradiation. Complex I and II substrate driven mitochondrial respiration was higher than controls at 72 h after irradiation, whereas complex IV substrate respiration decreased at 1 hour after irradiation but increased to control levels 48 h post-irradiation. ROS emission levels increased 1 h after irradiation, but returned to control levels at the 48 h post-irradiation time point. These data show that mild exposure of ROS benefits mitochondrial respiratory performance. Moreover, this study also provides a framework for future studies investigating the mitohormetic response.
