Abstract：
In the aquatic environment, the primary pollutants of heavy metals and pharmaceuticals always occur in coexisting forms, and the research about combined impacts remains unclear, especially transgenerational effects. Cadmium (Cd) is a heavy metal that can damage the endocrine reproduction systems and cause thyroid dysfunction in fish. Meanwhile, ketoprofen (KPF) is a nonsteroidal anti-inflammatory drug (NSAID) that can cause neurobehavioral damage and physiological impairment. However, to our knowledge, the combined exposure of Cd and KPF in transgenerational studies has not been reported. In this investigation, sexually mature zebrafish were subjected to isolated exposure and combined exposure to Cd (10 μg/L) and KPF (10 and 100 μg/L) at environmentally relevant concentrations for 42 days. In this background, breeding capacity, chemical accumulation rate in gonads, and tissue morphologies are investigated in parental fish. This is followed by examining the malformation rate, inflammation rate, and gene transcription in the F1 offspring. Our results indicate that combined exposure of Cd and KPF to the parental fish could increase the chemical accumulation rate and tissue damage in the gonads of fish and significantly reduce the breeding ability. Furthermore, these negative impacts were transmitted to its produced F1 embryos, reflected by hatching rate, body deformities, and thyroid axis-related gene transcription. These findings provide further insights into the harm posed by Cd in the presence of KPF to the aquatic ecosystems.
摘要：
在水生环境中，重金属和药物的主要污染物总是以共存的形式存在，关于综合影响的研究仍不清楚，尤其是跨代效应。镉（Cd）是一种重金属，可破坏鱼类的内分泌生殖系统并导致甲状腺功能异常。同时,酮洛芬（KPF）是一种非甾体抗炎药（NSAID），可引起神经行为损害和生理损害。然而,根据我们的知识，在跨代研究中Cd和KPF的联合暴露尚未报道。在这次调查中,对性成熟的斑马鱼进行隔离暴露，并以环境相关浓度暴露于Cd（10μg/L）和KPF（10和100μg/L），持续42天。在这样的背景下,繁殖能力，性腺中的化学积累速率，并在亲本鱼类中研究了组织形态。接下来是检查畸形率，炎症率，和F1后代的基因转录。我们的结果表明，Cd和KPF对亲本鱼类的联合暴露会增加鱼类性腺中的化学积累速率和组织损伤，并显着降低繁殖能力。此外，这些负面影响被传递给它生产的F1胚胎，由孵化率反映，身体畸形,和甲状腺轴相关基因转录。这些发现为在KPF存在下Cd对水生生态系统的危害提供了进一步的见解。
