Due to ineffective wastewater treatment technologies, pharmaceuticals such as the selective serotonin reuptake inhibitors (SSRIs)—a common class of antidepressants which inhibit the serotonin transporter (SERT)—can be found in surface waters and marine receiving waters near wastewater effluents. Understanding how exposure to these chemicals might impact non-target organisms, especially combined with other environmental stressors like hypoxia, is essential in order to thoroughly evaluate environmental risk. It was hypothesized that both acute and chronic exposure to the SSRI fluoxetine (FLX) would interfere with the metabolic hypoxia response of the Gulf toadfish, Opsanus beta. Here we demonstrate that acute intraperitoneal treatment with 50 μg g⁻¹ FLX significantly reduces the regulation index, or degree of metabolic regulation, in toadfish. Acute FLX exposure significantly reduced SERT mRNA expression in the first and third gill arches, but mRNA expression was not affected in heart tissues or in the second gill arch. In contrast, the regulation index was unaffected by 14–17 day waterborne FLX exposure to environmentally relevant (0.01 μg L⁻¹) and approximately 1000-fold higher (8.5 μg L⁻¹) concentrations. However, the higher concentration was sufficient to induce a systemic elevation in plasma serotonin concentrations. Chronic FLX exposure did not alter SERT mRNA expression in heart or gill tissues. The results of this study implicate the involvement of 5-HT pathways in hypoxia tolerance but demonstrate that current environmental levels of FLX are insufficient to impair the metabolic hypoxia response in marine fish.

由于无效的废水处理技术，在废水附近的地表水和海洋接收水中可以找到诸如5-羟色胺再摄取抑制剂（SSRIs）这类抑制5-羟色胺转运蛋白（SERT）的常见抗抑郁药。为了全面评估环境风险，了解与这些化学物质的接触可能如何影响非目标生物，尤其是与其他环境应激因素（如缺氧）相结合，至关重要。据推测，急性和慢性暴露于SSRI氟西汀（FLX）都会干扰海湾蟾蜍鱼Opsanus beta的代谢性缺氧反应。在这里，我们证明了用50μgg ^-1进行的急性腹膜内治疗FLX显着降低了蟾蜍的调节指数或代谢调节程度。急性FLX暴露显着降低了第一和第三腮弓中SERT mRNA的表达，但在心脏组织或第二腮弓中mRNA的表达没有受到影响。相比之下，调节指数不受与环境相关的（0.01μgL ^-1）和14-17天的水性FLX暴露的影响，并且大约高出1000倍（8.5μgL ^-1））浓度。但是，较高的浓度足以引起血浆5-羟色胺浓度的全身升高。慢性FLX暴露不会改变心脏或g组织中SERT mRNA的表达。这项研究的结果暗示5-HT途径参与了低氧耐受性，但表明当前环境水平的FLX不足以削弱海水鱼类的代谢性低氧反应。