Exposure to certain anthropogenic chemicals can inhibit the activity to cytochrome P450 aromatase (CYP19) in fishes leading to decreased plasma 17β-estradiol (E2), plasma vitellogenin (VTG), and egg production. Reproductive dysfunction resulting from exposure to aromatase inhibitors has been extensively investigated in several laboratory model species of fish. These model species have ovaries that undergo asynchronous oocyte development, but many fishes have ovaries with group-synchronous oocyte development. Fishes with group-synchronous oocyte development have dynamic reproductive cycles which typically occur annually and are often triggered by complex environmental cues. This has resulted in a lack of test data and uncertainty regarding sensitivities to and adverse effects of aromatase inhibition. The present study used the western mosquitofish (Gambusia affinis) as a laboratory model to investigate adverse effects of chemical aromatase inhibition on group-synchronous oocyte development. Adult female western mosquitofish were exposed to either 0, 2, or 30 μg/L of the model nonsteroidal aromatase inhibiting chemical, fadrozole, for a complete reproductive cycle. Fish were sampled at four time-points representing pre-vitellogenic resting, early vitellogenesis, late vitellogenesis/early ovarian recrudescence, and late ovarian recrudescence. Temporal changes in numerous reproductive parameters were measured, including gonadosomatic index (GSI), plasma sex steroids, and expression of selected genes in the brain, liver, and gonad that are important for reproduction. In contrast to fish from the control treatment, fish exposed to 2 and 30 μg/L of fadrozole had persistent elevated expression of cyp19 in the ovary, depressed expression of vtg in the liver, and a low GSI. These responses suggest that completion of a group-synchronous reproductive cycle was unsuccessful during the assay in fish from either fadrozole treatment. These adverse effects data show that exposure to aromatase inhibitors has the potential to cause reproductive dysfunction in a wide range of fishes with both asynchronous and group-synchronous reproductive strategies.

接触某些人为化学物质会抑制鱼类细胞色素 P450 芳香酶 (CYP19) 的活性，导致血浆 17β-雌二醇 (E2)、血浆卵黄蛋白原 (VTG) 和产蛋量下降。因接触芳香酶抑制剂而导致的生殖功能障碍已在几种实验室模型鱼类中进行了广泛研究。这些模式物种的卵巢进行异步卵母细胞发育，但许多鱼类的卵巢进行群体同步卵母细胞发育。具有群体同步卵母细胞发育的鱼类具有动态生殖周期，通常每年发生一次，并且通常由复杂的环境因素触发。这导致缺乏测试数据以及芳香酶抑制的敏感性和副作用的不确定性。本研究使用西方食蚊鱼（ Gambusia affinis ）作为实验室模型，研究化学芳香酶抑制对群体同步卵母细胞发育的不利影响。将成年雌性西部蚊鱼暴露于 0、2 或 30 μg/L 的模型非甾体芳香酶抑制化学物质法屈唑，以实现完整的繁殖周期。在代表卵黄发生前静息、早期卵黄发生、晚期卵黄发生/早期卵巢复发和晚期卵巢复发的四个时间点对鱼取样。测量了许多生殖参数的时间变化，包括性腺体指数（GSI）、血浆性类固醇以及大脑、肝脏和性腺中对生殖重要的选定基因的表达。 与对照处理的鱼相比，暴露于 2 和 30 μg/L 法屈唑的鱼卵巢中cyp19的表达持续升高，肝脏中vtg的表达降低，并且 GSI 较低。这些反应表明，在对接受任一法屈唑治疗的鱼进行测定时，组同步繁殖周期的完成并不成功。这些不利影响数据表明，接触芳香酶抑制剂有可能导致采用异步和群体同步繁殖策略的多种鱼类的繁殖功能障碍。