Selenium (Se) is considered an essential trace element, involved in important physiological and metabolic functions for all vertebrate species. Fish require dietary concentrations of 0.1–0.5 μg Se/g dry mass (d.m.) to maintain normal physiological and selenoprotein function, however concentrations exceeding 3 μg/g d.m. have been shown to cause toxicity. As Se is reported to have a narrow margin between essentiality and toxicity, there is growing concern surrounding the adverse effects of elevated Se exposure caused by anthropogenic activities. Previous studies have reported that elevated dietary exposure of fish to selenomethionine (Se-Met) can cause significant cardiotoxicity and alter aerobic metabolic capacity, energy homeostasis and swimming performance. The goal of this study aims to further investigate mechanisms of sublethal Se-Met toxicity, particularly potential underlying cardiovascular and metabolic implications of chronic exposure to environmentally relevant concentrations of dietary Se-Met in juvenile rainbow trout (Oncorhynchus mykiss). Juvenile rainbow trout were fed either control food (1.3 μg Se/g d.m.) or Se-Met spiked food (6.4, 15.8 or 47.8 μg Se/g d.m.) for 60 d at 3% body weight per day. Following exposure, ultrahigh resolution B-mode and Doppler ultrasound was used to characterize cardiac function in vivo. Chronic dietary exposure to Se-Met significantly increased stroke volume, cardiac output, and ejection fraction. Fish fed with Se-Met spiked food had elevated liver glycogen and triglyceride stores, suggesting impaired energy homeostasis. Exposure to Se-Met significantly decreased mRNA abundance of citrate synthase (CS) in liver and serpin peptidase inhibitor, clad H1 (SERPINH) in heart, and increased mRNA abundance of sarcoplasmic reticulum calcium ATPase (SERCA) and key cardiac remodelling enzyme matrix metalloproteinase 9 (MMP9) in heart. Taken together, these responses are consistent with a compensatory cardiac response to increased susceptibility to oxidative stress, namely a decrease in ventricular stiffness and improved cardiac function. These cardiac alterations in trout hearts were linked to metabolic disruption in other major metabolic tissues (liver and skeletal muscle), impaired glucose tolerance with increased levels of the toxic glucose metabolite, methylglyoxal, increased lipid peroxidation in skeletal muscle, development of cataracts and prolonged feeding behaviour, indicative of visual impairment. Therefore, although juvenile rainbow trout hearts were apparently able to functionally compensate for adverse metabolic and anti-oxidant changes after chronic dietary exposure Se-Met, complications associated with hyperglycemia in mammalian species were evident and would threaten survival of juvenile and adult fish.

硒（Se）被认为是必需的微量元素，参与所有脊椎动物物种的重要生理和代谢功能。鱼类需要0.1-0.5μg硒/克干质量（dm）的日粮浓度来维持正常的生理和硒蛋白功能，但是已经证明，浓度超过3μg/ g dm会引起毒性。据报道，由于硒在必需品和毒性之间的限度很小，因此人们越来越关注由人为活动引起的硒暴露增加带来的不利影响。先前的研究报告表明，鱼类饮食中硒代蛋氨酸（Se-Met）的暴露量增加会导致严重的心脏毒性，并改变有氧代谢能力，能量稳态和游泳能力。这项研究的目的旨在进一步研究亚致死性Se-Met毒性的机制，Oncorhynchus mykiss）。每天以3％的体重喂食幼年虹鳟鱼对照食物（1.3μgSe / g dm）或Se-Met加标食物（6.4、15.8或47.8μgSe / g dm）。暴露后，使用超高分辨率B型和多普勒超声表征体内心脏功能。长期饮食中Se-Met的暴露显着增加中风量，心输出量和射血分数。用Se-Met加标食品喂养的鱼肝糖原和甘油三酸酯含量升高，表明能量体内平衡受损。暴露于Se-Met会显着降低肝脏中柠檬酸合酶（CS）的mRNA丰度和心脏中Serpin肽酶抑制剂，包覆的H1（SERPINH）的mRNA含量，并增加肌浆网钙ATPase（SERCA）和关键的心脏重构酶基质金属蛋白酶9的mRNA含量（MMP9）放在心上。综上所述，这些反应与对氧化应激敏感性增加的代偿性心脏反应一致，即心室僵硬度降低和心脏功能改善。鳟鱼心脏的这些心脏变化与其他主要代谢组织（肝脏和骨骼肌）的代谢紊乱，葡萄糖耐量降低，毒性葡萄糖代谢产物，甲基乙二醛的含量增加，骨骼肌脂质过氧化作用增加，白内障的发生和进食时间延长有关行为，指示视力障碍。因此，尽管幼虹鳟鱼心脏在慢性饮食中接触Se-Met后显然能够在功能上补偿不利的代谢和抗氧化变化，但与哺乳动物高血糖相关的并发症却很明显，并且会威胁到幼鱼和成鱼的生存。骨骼肌脂质过氧化增加，白内障发展和进食行为延长，表明视力障碍。因此，尽管幼虹鳟鱼心脏在慢性饮食中接触Se-Met后显然能够在功能上补偿不利的代谢和抗氧化变化，但与哺乳动物高血糖相关的并发症却很明显，并且会威胁到幼鱼和成鱼的生存。骨骼肌脂质过氧化增加，白内障发展和进食行为延长，表明视力障碍。因此，尽管幼虹鳟鱼心脏在慢性饮食中接触Se-Met后显然能够在功能上补偿不利的代谢和抗氧化变化，但与哺乳动物高血糖相关的并发症却很明显，并且会威胁到幼鱼和成鱼的生存。