Toxicology Centre, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.
Aquat Toxicol. 2013 Apr 15;130-131:112-22. doi: 10.1016/j.aquatox.2013.01.009. Epub 2013 Feb 1.
In a previous study we reported impaired swimming performance and greater stored energy in adult zebrafish (Danio rerio) after chronic dietary exposure to selenomethionine (SeMet). The goal of the present study was to further investigate effects of chronic exposure to dietary SeMet on repeat swimming performance, oxygen consumption (MO2), metabolic capacities (standard metabolic rate [SMR], active metabolic rate [AMR], factorial aerobic scope [F-AS] and cost of transport [COT]) and gene expression of energy metabolism and methionine catabolism enzymes in adult zebrafish. Fish were fed SeMet at measured concentrations of 1.3, 3.4, 9.8 or 27.5 μg Se/g dry mass (d.m.) for 90 d. At the end of the exposure period, fish from each treatment group were divided into three subgroups: (a) no swim, (b) swim, and (c) repeat swim. Fish from the no swim group were euthanized immediately at 90 d and whole body triglycerides, glycogen and lactate, and gene expression of energy metabolism and methionine catabolism enzymes were determined. Individual fish from the swim group were placed in a swim tunnel respirometer and swimming performance was assessed by determining the critical swimming speed (U(crit)). After both Ucrit and MO2 analyses, fish were euthanized and whole body energy stores and lactate were determined. Similarly, individual fish from the repeat swim group were subjected to two U(crit) tests (U(crit-1) and U(crit-2)) performed with a 60 min recovery period between tests, followed by determination of energy stores and lactate. Impaired swim performance was observed in fish fed SeMet at concentrations greater than 3 μg Se/g in the diet. However, within each dietary Se treatment group, no significant differences between single and repeat U(crits) were observed. Oxygen consumption, SMR and COT were significantly greater, and F-AS was significantly lesser, in fish fed SeMet. Whole body triglycerides were proportional to the concentration of SeMet in the diet. While swimming resulted in lesser concentrations of glycogen in the body, exposure to SeMet in the diet had no significant effect on glycogen content. Exposure to SeMet significantly down-regulated mRNA abundance of protein tyrosine phosphatase 1B (PTP 1B) in muscle, and β-hydroxyacyl coenzyme A dehydrogenase (HOAD), sterol regulatory element binding protein 1 (SREBP 1) and methionine adenosyltransferase 1 alpha (MAT 1A) in liver of adult zebrafish. Overall the results of this study suggest chronic exposure of adult zebrafish to SeMet in the diet can cause both cellular and organismal effects that could affect fitness and survivability of fish.
在之前的研究中，我们报道了慢性饮食暴露于硒蛋氨酸（SeMet）后成年斑马鱼（Danio rerio）的游泳性能受损和储能增加。本研究的目的是进一步研究慢性饮食暴露于 SeMet 对成年斑马鱼重复游泳性能、耗氧量（MO2）、代谢能力（标准代谢率[SMR]、主动代谢率[AMR]、有氧范围因子[F-AS]和运输成本[COT]）以及能量代谢和蛋氨酸分解代谢酶基因表达的影响。鱼用测量浓度的 SeMet 喂养 1.3、3.4、9.8 或 27.5μg Se/g 干物质（d.m.）90d。在暴露期结束时，每组鱼分为三个亚组：（a）不游泳，（b）游泳，和（c）重复游泳。不游泳组的鱼在 90d 时立即安乐死，测定全身甘油三酯、糖原和乳酸，以及能量代谢和蛋氨酸分解代谢酶的基因表达。游泳组的个别鱼被放入游泳隧道呼吸计中，通过确定临界游泳速度（Ucrit）来评估游泳性能。在进行 MO2 分析后，对鱼进行安乐死，并测定全身能量储存和乳酸。同样，重复游泳组的个别鱼接受两次 U(crit) 测试（U(crit-1)和 U(crit-2)），两次测试之间有 60 分钟的恢复期，然后测定能量储存和乳酸。在饮食中 SeMet 浓度大于 3μg/g 时，鱼的游泳性能受损。然而，在每个饮食 Se 处理组中，单次和重复 U(crits)之间没有观察到显著差异。耗氧量、SMR 和 COT 显著增加，F-AS 显著降低，而饮食中 SeMet 的鱼则显著增加。全身甘油三酯与饮食中 SeMet 的浓度成正比。虽然游泳导致体内糖原浓度降低，但饮食中 SeMet 的暴露对糖原含量没有显著影响。暴露于 SeMet 显著下调了成年斑马鱼肌肉中蛋白酪氨酸磷酸酶 1B（PTP 1B）和肝脏中β-羟酰基辅酶 A 脱氢酶（HOAD）、固醇调节元件结合蛋白 1（SREBP 1）和蛋氨酸腺苷转移酶 1α（MAT 1A）的 mRNA 丰度。总的来说，这项研究的结果表明，成年斑马鱼慢性饮食暴露于 SeMet 会引起细胞和机体的影响，从而影响鱼类的适应性和生存能力。
