Monobutyl phthalate (MBP) is a primary metabolite of an environmental endocrine disruptor dibutyl phthalate (DBP), which poses a potential threat to living organisms. In this research, the acute toxicity of MBP on energy metabolism in zebrafish gills was studied. Transmission electron microscopy (TEM) results show that 10 mg L^-1 MBP can induce mitochondrial structural damage of chloride cells after 96 h of continuous exposure. The activity of ion ATPase and the expression level of oxidative phosphorylation-related genes suggest that MBP interferes with ATP synthesis and ion transport. Further leading to a decrease in mitochondrial membrane potential (MMP) and cell viability, thereby mediating early-stage cell apoptosis. Through a comprehensive analysis of principal component analysis (PCA) and integrated biomarker response (IBR) scores, atp5a1, a subunit of mitochondrial ATP synthase, is mainly inhibited, followed by genes encoding ion ATPase (atp1b2 and atp2b1). Importantly, MBP inhibits aerobic metabolism by inhibiting the key enzyme malate dehydrogenase (MDH) in the TCA cycle, forcing zebrafish to maintain ATP supply by enhancing anaerobic metabolism.

邻苯二甲酸单丁酯（MBP）是环境内分泌干扰物邻苯二甲酸二丁酯（DBP）的主要代谢产物，对生命有机体构成潜在威胁。在这项研究中，研究了MBP对斑马鱼g能量代谢的急性毒性。透射电子显微镜（TEM）结果显示10 mg L ^-1连续暴露96小时后，MBP可以诱导氯化物细胞的线粒体结构损伤。离子ATPase的活性和氧化磷酸化相关基因的表达水平表明MBP干扰ATP的合成和离子运输。进一步导致线粒体膜电位（MMP）和细胞活力降低，从而介导早期细胞凋亡。通过对主成分分析（PCA）和综合生物标记反应（IBR）得分的综合分析，主要抑制了线粒体ATP合酶亚基的atp5a1，其次是编码离子ATPase的基因（atp1b2和atp2b1）。重要的是，MBP通过抑制TCA循环中的关键酶苹果酸脱氢酶（MDH）来抑制有氧代谢，从而迫使斑马鱼通过增强无氧代谢来维持ATP的供应。