P2.180 Thursday, Jan. 5 Prenatal exposure to testosterone mitigates the stress-induced rise in oxidative stress in domestic chickens (Gallus gallus) TREIDEL, L.A.*; WHITLEY, B.N.; BENOWITZ-FREDERICKS, Z.M.; HAUSSMANN, M.F.; Bucknell Univ., Lewisburg; Bucknell Univ., Lewisburg; Bucknell Univ., Lewisburg; Bucknell Univ., Lewisburg email@example.com
Elevated levels of maternally deposited androgens in avian eggs impact several offspring traits, such as begging behavior, metabolic rate, and growth during early development. Prenatal androgens also influence oxidative stress. Current studies, however, disagree whether their impact is beneficial or costly, with some reporting increased oxidative stress resistance and others reporting increased levels of oxidative damage. Previous work in our lab has shown that during an acute stress response, birds’ shift into a state of oxidative stress with increased oxidative damage and decreased antioxidant defense. Here, we tested how prenatal testosterone exposure would impact the stress-induced rise in oxidative stress in female domestic chickens (Gallus gallus). Prior to incubation, eggs were either injected with an oil vehicle (n=10) or testosterone (5ng, n=10). At either 18 or 19 days post hatch, all birds were subjected to an acute stress series and blood samples were taken at <3, 20, and 45 min. Baseline oxidative damage to erythrocyte DNA, vulnerability of DNA to a hydrogen-peroxide challenge, and DNA repair capabilities following the challenge were assessed for all blood samples using the single cell gel electrophoresis assay. We found that regardless of yolk treatment, after the first 20 min of the stress response all birds had increased levels of DNA damage, but control birds experienced more DNA damage than testosterone birds. Our work suggests that while yolk androgens can increase metabolic rate, which is known to elevate oxidative stress, prenatal testosterone exposure can also protect against oxidative stress by mitigating stress-induced oxidative damage to DNA.