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ABSTRACT The ability of organisms to effectively respond to challenges is critical for survival. We investigated how an acute stressor affected corticosterone, mitochondrial function, and DNA oxidative damage in a wild population of Leach's storm‐petrels (Hydrobates leucorhous). We conducted a standardized 20‐min handling procedure on storm‐petrel chicks and collected baseline and post‐handling blood samples. We measured plasma corticosterone and red blood cell DNA oxidative damage levels through the detection of a mutated DNA base 8‐Hydroxy‐2'‐deoxyguanosine (8‐OHdG). In addition, we quantified six measures of mitochondrial aerobic metabolism from red blood cells. Overall, the handling stressor increased plasma corticosterone levels and decreased mitochondrial efficiency to produce ATP. Although the increase in corticosterone was inversely related to the change in DNA oxidative damage, the decrease in mitochondrial efficiency was positively correlated with the change in DNA oxidative damage. Thus, over an acute stress response, individuals who had the largest increase in corticosterone also had the least amount of oxidative damage. In addition, individuals who prioritized ATP production during the acute stress also showed higher levels of oxidative damage. This work highlights the complex pathways by which corticosterone and mitochondrial efficiency affect oxidative damage during acute stress, providing new insights into the trade‐offs underlying physiological responses in wild animals.