Meeting Abstract
Oxidative stress has been proposed as a mediator underlying different life-history trade-offs. Evolutionary physiologists often assume mitochondria as the center of release and regulation of reactive oxygen species (ROS) levels. Unfortunately, evidences for such an assumption were limited since ROS production levels from different cellular compartments in intact cells were difficult to quantify. Previous studies relied heavily on intracellular fluorescent probes, but such probes are only useful for qualitative rather than quantification of ROS. In the present study, we employed a newly developed method to accurately quantify ROS production from different cellular compartments. We surveyed a large variety of cell types including primary cells from different tissues of various species. Moreover, we also measured changes in ROS profile during tunicamycin induced ER stress as an example for a stress model. Overall, the significance of mitochondria ROS production varies between cell types, with their contribution to total cellular ROS production being less than 50% in majority, but H9c2 cardiomyocytes, of cell types. On the other hand, other cellular compartments such as NADPH oxidases contributed a major portion of ROS production in some cell types under unstressed conditions. These data show mitochondria are not the major site of ROS production in all cell types. As a result, when studying life-history trade-offs, we must be cautious and should not always assume ROS production comes from mitochondria.
