School of Marine Science and Engineering, Qingdao Agricultural University, No. 17 Wenhai Road, Qingdao, China; Laboratory for Marine Ecology and Environmental Science, Laoshan Laboratory, No. 1 Wenhai Road, Qingdao, China.
Department of Marine Ecology, College of Marine Life Sciences, Ocean University of China, No. 5 Yushan Road, Qingdao, China; Laboratory for Marine Ecology and Environmental Science, Laoshan Laboratory, No. 1 Wenhai Road, Qingdao, China.
Sci Total Environ. 2023 Aug 10;885:163766. doi: 10.1016/j.scitotenv.2023.163766. Epub 2023 May 3.
The energetic response of blue mussel Mytilus edulis when coping with tetrabromodiphenyl ether (BDE-47) exposure was evaluated from the perspective of alterations in energy supply mode, and the possible regulating mechanism was discussed based on a 21-day bioassay. The results showed that the energy supply mode changed with concentration: 0.1 μg/L BDE-47 decreased the activity of isocitrate dehydrogenase (IDH), succinate dehydrogenase (SDH), malate dehydrogenase and oxidative phosphorylation, suggesting inhibition of the tricarboxylic (TCA) acid cycle and aerobic respiration. The coincident increase in phosphofructokinase and the decrease in lactate dehydrogenase (LDH) indicated that glycolysis and anaerobic respiration were increased. When exposed to 1.0 μg/L BDE-47, M. edulis mainly utilized aerobic respiration, but lowered glucose metabolism as indicated by the decrease in glutamine and l-leucine was suggested to be involved in this process, which was differed from that in the control. The reoccurrence of IDH and SDH inhibition as well as LDH elevation indicated attenuation of aerobic and anaerobic respiration when the concentration increased to 10 μg/L, but severe protein damage was evidenced based on the elevation of amino acids and glutamine. Under the 0.1 μg/L BDE-47, activation of the AMPK-Hif-1a signaling pathway promoted the expression of glut1, which was the potential mechanism for the improvement of anaerobic respiration, and further activated glycolysis and anaerobic respiration. This study shows that the energy supply mode experienced a conversion from aerobic respiration under normal conditions to anaerobic mode in the low BDE-47 treatment and back to aerobic respiration with increasing BDE-47 concentrations, which may represent a potential mechanism for mussel physiological responses when faced with different levels of BDE-47 stress.
当贻贝应对四溴二苯醚 (BDE-47) 暴露时，从能量供应模式改变的角度评估了其活力响应，并基于 21 天的生物测定讨论了可能的调节机制。结果表明，随着浓度的变化，贻贝的能量供应模式发生了改变：0.1μg/L 的 BDE-47 降低了异柠檬酸脱氢酶（IDH）、琥珀酸脱氢酶（SDH）、苹果酸脱氢酶和氧化磷酸化的活性，表明三羧酸（TCA）循环和需氧呼吸受到抑制。磷酸果糖激酶的协同增加和乳酸脱氢酶（LDH）的减少表明糖酵解和无氧呼吸增加。当暴露于 1.0μg/L 的 BDE-47 时，贻贝主要利用需氧呼吸，但降低了葡萄糖代谢，表明谷氨酰胺和亮氨酸的减少参与了这一过程，这与对照组不同。当浓度增加到 10μg/L 时，IDH 和 SDH 抑制以及 LDH 升高再次表明需氧和无氧呼吸的减弱，但氨基酸和谷氨酰胺的升高表明蛋白质严重受损。在 0.1μg/L 的 BDE-47 下，AMPK-Hif-1a 信号通路的激活促进了 glut1 的表达，这是改善无氧呼吸的潜在机制，并进一步激活了糖酵解和无氧呼吸。本研究表明，在正常条件下，贻贝的能量供应模式从需氧呼吸转变为低 BDE-47 处理下的无氧模式，随着 BDE-47 浓度的增加，恢复到需氧呼吸，这可能代表贻贝在面对不同水平的 BDE-47 胁迫时生理反应的潜在机制。
