The co-occurrence of hypoxia and xenobiotics is extremely common in natural environments, highlighting the necessity to elicit their interaction on aquatic toxicities. In the present study, marine medaka embryos were exposed to various concentrations (nominal 0, 1, 3.3 and 10 mg/L) of perfluorobutane sulfonate (PFBS), an environmental pollutant of emerging concern, under either normoxia (6.9 mg/L) or hypoxia (1.7 mg/L) condition. After acute exposure till 15 days post-fertilization, single or combined toxicities of PFBS and hypoxia on embryonic development (e.g., mortality, hatching and heartbeat) and endocrine systems were investigated. Sex and thyroid hormones were measured by enzyme-linked immunosorbent assay. Transcriptional changes of endocrine genes were determined by quantitative real-time PCR assays. Co-exposure to 10 mg/L PFBS and hypoxia caused a further reduction in survival rate and heart beat compared to single exposure. PFBS induced a precocious hatching, while no larvae hatched under hypoxia condition. By disturbing the balance of sex hormones, either PFBS or hypoxia single exposure produced an anti-estrogenic activity in medaka larvae. However, PFBS and hypoxia combinations reversed to estrogenic activity in co-exposed larvae. Variation in disrupting pattern may be attributed to the interactive effects on steroidogenic pathway involving diverse cytochrome P450 enzymes. Regarding thyroid system, PFBS exposure caused detriments of multiple processes along thyroidal axis (e.g., feedback regulation, synthesis and transport of thyroid hormones, receptor-mediated signaling and thyroid gland development), while hypoxia potently impaired the development and function of thyroid gland. Combinations of PFBS and hypoxia interacted to dysregulate the function of thyroid endocrine system. In summary, the present study revealed the dynamic interaction of PFBS pollutant and hypoxia on aquatic developmental toxicities and endocrine disruption. Considering the frequent co-occurrence of xenobiotics and hypoxia, current results would be beneficial to improve our understanding about their interactive mechanisms and provide baseline evidences for accurate ecological risk evaluation.

中文翻译：

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低氧和全氟丁烷磺酸盐对海洋中高加索胚胎发育毒性和内分泌干扰的相互作用。

在自然环境中，低氧和异源生物并存是非常普遍的现象，这突出了引起它们对水生毒性的相互作用的必要性。在本研究中，海洋常绿胚胎在常氧（6.9 mg / L）或高温下暴露于各种浓度的（名义上的0、1、3.3和10 mg / L）全氟丁烷磺酸盐（PFBS），一种新出现的环境污染物。低氧（1.7 mg / L）条件。急性暴露后直至受精后15天，研究了PFBS和低氧对胚胎发育（例如，死亡率，孵化率和心跳）和内分泌系统的单一或联合毒性。通过酶联免疫吸附法测定性激素和甲状腺激素。内分泌基因的转录变化通过定量实时PCR测定来确定。与单次暴露相比，同时暴露于10 mg / L PFBS和缺氧会导致存活率和心跳进一步降低。PFBS引起早熟孵化，而在低氧条件下没有幼虫孵化。通过扰乱性激素的平衡，PFBS或缺氧单次接触都会对高幼虫产生抗雌激素活性。然而，PFBS和缺氧组合可逆转共暴露幼虫的雌激素活性。破坏模式的变化可能归因于涉及多种细胞色素P450酶的类固醇生成途径的相互作用。关于甲状腺系统，全氟辛烷磺酸暴露导致沿甲状腺轴的多个过程受到损害（例如，反馈调节，甲状腺激素的合成和运输，受体介导的信号传导和甲状腺发育），缺氧会严重损害甲状腺的发育和功能。PFBS和缺氧的组合相互作用，从而异常调节甲状腺内分泌系统的功能。总之，本研究揭示了PFBS污染物与缺氧对水生发育毒性和内分泌干扰的动态相互作用。考虑到异种生物和缺氧的频繁发生，当前的结果将有助于增进我们对它们的相互作用机制的理解，并为准确的生态风险评估提供基线证据。本研究揭示了PFBS污染物和缺氧对水生发育毒性和内分泌干扰的动态相互作用。考虑到异种生物和缺氧的频繁发生，当前的结果将有助于增进我们对它们的相互作用机制的理解，并为准确的生态风险评估提供基线证据。本研究揭示了PFBS污染物和缺氧对水生发育毒性和内分泌干扰的动态相互作用。考虑到异种生物和缺氧的频繁发生，当前的结果将有助于增进我们对它们的相互作用机制的理解，并为准确的生态风险评估提供基线证据。