Data from: An experimental test of the testosterone mediated oxidation handicap hypothesis in a wild bird

The oxidation handicap hypothesis (OHH) proposed that honesty in sexual signals is maintained when testosterone simultaneously promotes the development of elaborate signals and imposes an oxidative cost. Although there is evidence that testosterone enhances display traits in some cases, relatively few studies have tested the prediction that testosterone generates oxidative costs. We tested this prediction experimentally by administering testosterone (n = 14) and control (n = 14) implants to free-living common yellowthroat warblers (Geothlypis trichas) and quantifying testosterone and oxidative state before and 35 ± 15 days after implantation. We interpreted our experimental results in the context of a larger database of 83 unmanipulated males observed over five breeding seasons. In our observational data, testosterone was related to aspects of the carotenoid-based bib, but these relationships were age-dependent. Bib coloration was related to testosterone only for first time breeders, while bib size was positively and negatively associated with testosterone among experienced and inexperienced breeders, respectively. Two measures of oxidative metabolism—damage to DNA and total antioxidant capacity (TAC)—were unrelated to endogenous testosterone. Despite the correlation between endogenous testosterone and plumage, our experimental results failed to support the key prediction of the OHH. Testosterone treated males had higher levels of TAC upon recapture, but oxidative damage to DNA did not differ from controls. Because antioxidants can protect against the harmful effects of oxidative stress, one interpretation of our results is that males physiologically compensated for elevated testosterone, avoiding the honesty enforcing mechanism of the OHH. Taken together, our results suggest that testosterone is not a direct mediator of honest signaling in yellowthroats via its effects on oxidative stress.氧化障碍假说（oxidation handicap hypothesis, OHH）提出，当睾酮同时促进精致性信号的发育并施加氧化成本时，性信号的诚实性得以维持。尽管有证据表明睾酮在某些情况下会增强展示性状，但验证"睾酮会产生氧化成本"这一预测的研究相对较少。我们通过对自由生活的普通黄喉林莺（Geothlypis trichas）分别植入睾酮（n = 14）和对照（n = 14）植入剂，在植入前以及植入后35 ± 15天量化睾酮水平与氧化状态，以此实验检验该预测。我们结合5个繁殖季观测得到的83只未受干扰雄性的更大规模数据库来解读实验结果。在观测数据中，睾酮与基于类胡萝卜素的喉斑特征相关，但这些关联具有年龄依赖性。仅在首次繁殖个体中，喉斑色泽与睾酮相关；而在繁殖经验丰富与缺乏经验的个体中，喉斑大小分别与睾酮呈正相关与负相关。两项氧化代谢指标——DNA损伤与总抗氧化能力（total antioxidant capacity, TAC）——与内源性睾酮并无关联。尽管内源性睾酮与羽色存在相关性，但我们的实验结果未能支持氧化障碍假说的核心预测。经睾酮处理的雄性个体重捕时的总抗氧化能力水平更高，但DNA的氧化损伤与对照组并无差异。由于抗氧化物质可抵御氧化应激的有害影响，对我们的结果的一种解读是：雄性个体通过生理补偿应对升高的睾酮水平，从而规避了氧化障碍假说中维持诚实性的机制。综合来看，我们的结果表明，睾酮并未通过影响氧化应激直接介导黄喉林莺的诚实性信号传递。