Department of Pharmacology and Environmental Toxicology Research Program, School of Pharmacy, University of Mississippi, University, MS 38677, USA.
Department of Pharmacology and Environmental Toxicology Research Program, School of Pharmacy, University of Mississippi, University, MS 38677, USA.
Aquat Toxicol. 2014 Mar;148:16-26. doi: 10.1016/j.aquatox.2013.12.028. Epub 2014 Jan 3.
In the aquatic environment, adverse outcomes from dietary polycyclic aromatic hydrocarbon (PAH) exposure are poorly understood, and multigenerational developmental effects following exposure to PAHs are in need of exploration. Benzo[a]pyrene (BaP), a model PAH, is a recognized carcinogen and endocrine disruptor. Here adult zebrafish (F0) were fed 0, 10, 114, or 1,012 μg BaP/g diet at a feed rate of 1% body weight twice/day for 21 days. Eggs were collected and embryos (F1) were raised to assess mortality and time to hatch at 24, 32, 48, 56, 72, 80, and 96 h post fertilization (hpf) before scoring developmental deformities at 96 hpf. F1 generation fish were raised to produce the F2 generation followed by the F3 and F4 generations. Mortality significantly increased in the higher dose groups of BaP (2.3 and 20 μg BaP/g fish) in the F1 generation while there were no differences in the F2, F3, or F4 generations. In addition, premature hatching was observed among the surviving fish in the higher dose of the F1 generation, but no differences were found in the F2 and F3 generations. While only the adult F0 generation was BaP-treated, this exposure resulted in multigenerational phenotypic impacts on at least two generations (F1 and F2). Body morphology deformities (shape of body, tail, and pectoral fins) were the most severe abnormality observed, and these were most extreme in the F1 generation but still present in the F2 but not F3 generations. Craniofacial structures (length of brain regions, size of optic and otic vesicles, and jaw deformities), although not significantly affected in the F1 generation, emerged as significant deformities in the F2 generation. Future work will attempt to molecularly anchor the persistent multigenerational phenotypic deformities noted in this study caused by BaP exposure.
在水生环境中，饮食中多环芳烃（PAH）暴露的不良后果尚未被充分理解，而多代暴露于 PAHs 后的发育影响则需要进一步探索。苯并[a]芘（BaP）是一种典型的 PAH，被认为是一种致癌物质和内分泌干扰物。在这里，成年斑马鱼（F0）以 1%体重的饲料率，每天两次喂养 0、10、114 或 1012μg BaP/g 饮食 21 天。收集卵并孵育胚胎（F1），以评估受精后 24、32、48、56、72、80 和 96 小时的死亡率和孵化时间，然后在 96 小时时评估发育畸形。F1 代鱼类被饲养以产生 F2 代，然后是 F3 和 F4 代。在 F1 代中，BaP 的高剂量组（2.3 和 20μg BaP/g 鱼）死亡率显著增加，而在 F2、F3 和 F4 代中没有差异。此外，在 F1 代高剂量组的幸存鱼中观察到早产，但在 F2 和 F3 代中没有差异。尽管只有成年 F0 代接受了 BaP 处理，但这种暴露导致至少两代（F1 和 F2）的多代表型影响。身体形态畸形（身体、尾巴和胸鳍的形状）是观察到的最严重的异常，在 F1 代中最为严重，但在 F2 代中仍然存在，但在 F3 代中不存在。颅面结构（脑区长度、视囊和耳囊大小以及颌骨畸形）在 F1 代中没有受到显著影响，但在 F2 代中出现了显著的畸形。未来的工作将试图从分子水平上确定 BaP 暴露引起的本研究中持续存在的多代表型畸形。
