Monobutyl phthalate (MBP) can exist in biological organisms for a long time because of its excellent fat solubility, and it has been found to have certain toxic effects. In this study, the acute effects of MBP on endoplasmic reticulum (ER) stress and metabolism in the zebrafish liver were studied. After continuous exposure to MBP (5 and 10 mg / L) for 96 h, ER damage and the appearance of apoptotic bodies and autophagosomes were found in liver. This is because MBP stimulated the ire-xbp1 pathway of ER stress, thus leading to apoptosis and autophagy. Also, through analysis of metabolic enzymes and genes, it was found that the activated ire-xbp1 pathway could promote lipid synthesis and cause the accumulation of lipid droplets. The gene pparγ related to lipid storage affected the level of insulin, which can also further affect the glucose metabolism process, that is, glycolysis and aerobic respiration were inhibited. And the pentose phosphate pathway (PPP) was activated as a compensation mechanism to alleviate glycogen accumulation. The abnormal supply of energy and the death of excessive cells will eventually severely damage the zebrafish liver. This study will enrich the knowledge about the toxic effects of MBP.

邻苯二甲酸单丁酯（MBP）由于其极好的脂肪溶解性而可以在生物中长期存在，并且已发现具有一定的毒性作用。在这项研究中，研究了MBP对斑马鱼肝脏内质网（ER）应激和代谢的急性作用。连续暴露于MBP（5和10 mg / L）96 h后，在肝脏中发现了ER损伤以及凋亡小体和自噬小体的出现。这是因为MBP刺激ER应激的ire-xbp1途径，从而导致细胞凋亡和自噬。另外，通过对代谢酶和基因的分析，发现激活的ire-xbp1途径可以促进脂质合成并引起脂质液滴的积累。pparγ基因与脂质存储有关的胰岛素水平受到影响，这也可以进一步影响葡萄糖的代谢过程，即糖酵解和有氧呼吸被抑制。磷酸戊糖途径（PPP）被激活为补偿糖原积累的补偿机制。异常的能量供应和过多细胞的死亡最终将严重损害斑马鱼的肝脏。这项研究将丰富有关MBP毒性作用的知识。