Jordão Rita, Casas Josefina, Fabrias Gemma, Campos Bruno, Piña Benjamín, Lemos Marco F L, Soares Amadeu M V M, Tauler Romà, Barata Carlos
Department of Environmental Chemistry, Institute of Environmental Assessment and Water Research (IDAEA), Spanish Research Council (IDAEA, CSIC), Barcelona, Spain.
Environ Health Perspect. 2015 Aug;123(8):813-9. doi: 10.1289/ehp.1409163. Epub 2015 Mar 24.
The analysis of obesogenic effects in invertebrates is limited by our poor knowledge of the regulatory pathways of lipid metabolism. Recent data from the crustacean Daphnia magna points to three signaling hormonal pathways related to the molting and reproductive cycles [retinoic X receptor (RXR), juvenile hormone (JH), and ecdysone] as putative targets for exogenous obesogens.
The present study addresses the disruptive effects of the model obesogen tributyltin (TBT) on the lipid homeostasis in Daphnia during the molting and reproductive cycle, its genetic control, and health consequences of its disruption.
D. magna individuals were exposed to low and high levels of TBT. Reproductive effects were assessed by Life History analysis methods. Quantitative and qualitative changes in lipid droplets during molting and the reproductive cycle were studied using Nile red staining. Lipid composition and dynamics were analyzed by ultra-performance liquid chromatography coupled to a time-of-flight mass spectrometer. Relative abundances of mRNA from different genes related to RXR, ecdysone, and JH signaling pathways were studied by qRT-PCR.
TBT disrupted the dynamics of neutral lipids, impairing the transfer of triacylglycerols to eggs and hence promoting their accumulation in adult individuals. TBT's disruptive effects translated into a lower fitness for offspring and adults. Co-regulation of gene transcripts suggests that TBT activates the ecdysone, JH, and RXR receptor signaling pathways, presumably through the already proposed interaction with RXR. These findings indicate the presence of obesogenic effects in a nonvertebrate species.
对无脊椎动物致肥胖效应的分析受到我们对脂质代谢调节途径了解不足的限制。来自甲壳类动物大型溞的最新数据指出，与蜕皮和生殖周期相关的三种信号激素途径[视黄酸X受体（RXR）、保幼激素（JH）和蜕皮激素]可能是外源性致肥胖物的作用靶点。
本研究探讨了典型致肥胖物三丁基锡（TBT）在蜕皮和生殖周期对大型溞脂质稳态的破坏作用、其遗传控制以及破坏后的健康后果。
将大型溞个体暴露于低水平和高水平的TBT中。通过生活史分析方法评估生殖效应。使用尼罗红染色研究蜕皮和生殖周期中脂滴的定量和定性变化。通过超高效液相色谱与飞行时间质谱联用分析脂质组成和动态变化。通过qRT-PCR研究与RXR、蜕皮激素和JH信号通路相关的不同基因的mRNA相对丰度。
TBT破坏了中性脂质的动态变化，损害了三酰甘油向卵中的转运，从而促进其在成年个体中的积累。TBT的破坏作用导致后代和成年个体的适应性降低。基因转录本的共同调节表明，TBT可能通过已提出的与RXR的相互作用激活蜕皮激素、JH和RXR受体信号通路。这些发现表明在非脊椎动物物种中存在致肥胖效应。
