Prenatal exposure to testosterone impairs oxidative damage repair efficiency in the domestic chicken ( Gallus gallus )
Author(s) -
Lisa A. Treidel,
B. N. Whitley,
Z Morgan BenowitzFredericks,
Mark F. Haussmann
Publication year - 2013
Publication title -
biology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.596
H-Index - 110
eISSN - 1744-957X
pISSN - 1744-9561
DOI - 10.1098/rsbl.2013.0684
Subject(s) - biology , oxidative damage , testosterone (patch) , oxidative phosphorylation , prenatal exposure , oxidative stress , medicine , endocrinology , pregnancy , genetics , gestation , biochemistry
Elevated levels of maternal androgens in avian eggs affect numerous traits, including oxidative stress. However, current studies disagree as to whether prenatal androgen exposure enhances or ameliorates oxidative stress. Here, we tested how prenatal testosterone exposure affects oxidative stress in female domestic chickens (Gallus gallus) during the known oxidative challenge of an acute stressor. Prior to incubation, eggs were either injected with an oil vehicle or 5 ng testosterone. At either 17 or 18 days post-hatch, several oxidative stress markers were assessed from blood taken before and after a 20 min acute stressor, as well as following a 25 min recovery from the stressor. We found that, regardless of yolk treatment, during both stress and recovery all individuals were in a state of oxidative stress, with elevated levels of oxidative damage markers accompanied by a reduced total antioxidant capacity. In addition, testosterone-exposed individuals exhibited poorer DNA damage repair efficiencies in comparison with control individuals. Our work suggests that while yolk androgens do not alter oxidative stress directly, they may impair mechanisms of oxidative damage repair.
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