In this paper, the acute toxicity of monobutyl phthalate (MBP), the main hydrolysis product of dibutyl phthalate, on adult zebrafish liver antioxidant system was studied. Compared the toxicity effect of MBP and DBP by histopathology and apoptosis experiments, we speculated that the toxic effects of DBP on animals may be caused by its metabolite MBP. The results indicated that the antioxidant Nrf2-Keap1 pathway was insufficient to resist MBP-induced hepatotoxicity and led to an imbalance of membrane ion homeostasis and liver damage. Decreased cell viability, significant tissue lesions and early hepatocyte apoptosis were observed in the zebrafish liver in MBP exposure at high concentration (10 mg/L). The activities of antioxidant enzymes and ATPases in zebrafish liver were inhibited with increased malondialdehyde (MDA) content and alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities. Integrated biomarker response (IBR) calculation results indicated that MBP mainly inhibited catalase (CAT) activity. Simultaneously, the expression of antioxidant-related genes (SOD, CAT, GPx, Nrf2, HO-1) was down-regulated, while apoptosis-related genes (p53, bax, cas3) were significantly up-regulated.

中文翻译：

---

邻苯二甲酸单丁酯（MBP）会失调抗氧化系统并诱导斑马鱼肝脏凋亡。

本文研究了邻苯二甲酸二丁酯的主要水解产物邻苯二甲酸单丁酯（MBP）对成年斑马鱼肝脏抗氧化系统的急性毒性。通过组织病理学和凋亡实验比较了MBP和DBP的毒性作用，我们推测DBP对动物的毒性作用可能是由其代谢产物MBP引起的。结果表明，抗氧化剂Nrf2-Keap1途径不足以抵抗MBP诱导的肝毒性，并导致膜离子稳态和肝损伤的失衡。在高浓度（10 mg / L）的MBP暴露下，斑马鱼肝脏中观察到细胞活力降低，明显的组织损伤和早期肝细胞凋亡。丙二醛（MDA）含量和丙氨酸氨基转移酶（ALT）和天冬氨酸氨基转移酶（AST）活性均被抑制，从而抑制了斑马鱼肝脏中抗氧化酶和ATPase的活性。综合生物标志物响应（IBR）计算结果表明，MBP主要抑制过氧化氢酶（CAT）活性。同时，抗氧化剂相关基因（SOD，CAT，GPx，Nrf2，HO-1）的表达下调，而凋亡相关基因（p53，bax，cas3）的表达上调。