Meeting Abstract

P3.178  Sunday, Jan. 6  Stress management: How do repeated stressors affect antioxidant capacity and oxidative damage? FASANELLO, V,J.*; FISCHER, C.P.; FLETCHER, K.L.; MAKRIS, M.E.; SEECOF, O.M.; VASSALLO, B.G.; HAUSSMANN, M.F.; Bucknell Univ.; Bucknell Univ.; Bucknell Univ.; Bucknell Univ.; Bucknell Univ.; Bucknell Univ.; Bucknell Univ. mfh008@bucknell.edu

Oxidative respiration results in the production of reactive oxygen species (ROS), which can damage proteins, membranes, and DNA. Organisms have evolved mechanisms such as antioxidant defense to reduce ROS propagation and the oxidative damage that results. Nevertheless, oxidative damage still occurs, and the accumulation of this damage is a critical component of the aging process. Previous work has shown that antioxidant levels can increase or decrease over an acute stress response. Repeated stressors at a young age may prepare antioxidant defenses for subsequent stress responses by increasing antioxidant levels through hormesis. In contrast, repeated stressors at a young age could exhaust antioxidant stores to result in greater oxidative damage. We tested these predictions in one month old Japanese quail (Coturnix japonica) over a twenty-three day period by exposing them to differing numbers of the same acute stress protocol: high stress (H; a total of eight stressors), low stress (L; two stressors, the initial and final), and naïve (N; only the final stressor). Plasma levels of oxidative damage and total antioxidant capacity were measured from the final acute stress response. We found that over this stress response, antioxidant levels significantly decreased in the H birds, increased in the N birds, and was intermediate in the L birds. This experiment shows that repeated stressors can exhaust antioxidant stores, suggesting that animals living in natural populations experiencing high levels of environmental stress may have higher loads of oxidative stress and increased cellular aging.