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Meeting Abstract
P1.130 Saturday, Jan. 4 15:30 Glucocorticoid-induced Oxidative Stress (GiOS): cellular consequences to elevated glucocorticoids? FASANELLO, VJ*; VASSALLO, BG; FISCHER, CP; REED, WL; HAUSSMANN, MF; Bucknell Univ, Lewisburg; Bucknell Univ, Lewisburg; Bucknell Univ, Lewisburg; North Dakota State Univ, Fargo; Bucknell Univ, Lewisburg mfh008@bucknell.edu
During a stress response, elevated glucocorticoids alter the physiology and behavior of individuals, promoting survival in an unpredictable environment. Recent evidence, from our laboratory, suggests that glucocorticoid exposure during acute stress causes a shift into oxidative stress; a phenomenon we term Glucocorticoid-induced Oxidative Stress (GiOS). During oxidative stress, reactive oxygen species are produced which cause oxidative damage to macromolecules throughout the body, resulting in a decline in organismal performance and survival. We sought to characterize and explore GiOS through two experiments. First, we characterize GiOS in both domestic and feral breeds of Japanese quail (Coturnix japonica) during an acute stress response. Second, we explore how the pattern of stress affects GiOS in domestic quail. We found that, regardless of breed, plasma oxidative damage increased and plasma antioxidants decreased during an acute stress response. In our second experiment, we exposed groups of domestic quail to different patterns of the same acute stress protocol: high stress (8 stressors in 3 wk) and low stress (2 stressors in 3 wk). We found that plasma oxidative damage decreased in the low stress birds, but increased in the high stress birds, while plasma antioxidants increased in the low stress birds, but decreased in the high stress birds. Our results show that GiOS appears to be a conserved phenomenon in feral and domestic quail. Furthermore, we show that the pattern of stress is important. Low frequency of repeated stress appears to prime the system, protecting against oxidative damage, while high frequency of repeated stress increases oxidative damage.