Butyl benzyl phthalate (BBP), a typical phthalate plasticizer, is frequently detected in aquatic environments, but its possible effects on fish liver are unknown. In this study, adult zebrafish were exposed to 5–500 μg/L BBP and cultured for 28 days. The toxicity mechanism of environmentally relevant concentrations of BBP in the liver was explored using integrated biomarker response (IBR), molecular docking, and histopathological analysis, based on the tests of oxidative stress, apoptosis, and tissue damage, respectively. The results revealed that exposure to 500 μg/L BBP caused lipid peroxidation and DNA damage and induced inflammatory responses in the liver and intestinal tissues. The accumulation of reactive oxygen species (ROS) is the primary manifestation of BBP toxicity and is accompanied by changes in the activities of antioxidant and detoxification enzymes. Notably, the pro-apoptotic genes (p53 and caspase-3) were still significantly upregulated in the 50 μg/L and 500 μg/L treatment groups on day 28. Moreover, BBP interfered with apoptosis by forming a stable complex with apoptosis proteins (P53 and Caspase-3). Our findings are helpful for understanding the toxicity mechanisms of BBP, which could further promote the assessment of the potential environmental risks of BBP.

邻苯二甲酸丁苄酯 (BBP) 是一种典型的邻苯二甲酸酯增塑剂，经常在水生环境中检测到，但其对鱼肝的可能影响尚不清楚。在这项研究中，成年斑马鱼暴露于 5–500 μg/L BBP 并培养 28 天。基于氧化应激、细胞凋亡和组织损伤的测试，分别使用综合生物标志物反应 (IBR)、分子对接和组织病理学分析，探索环境相关浓度的 BBP 在肝脏中的毒性机制。结果表明，暴露于 500 μg/L BBP 会导致脂质过氧化和 DNA 损伤，并在肝脏和肠道组织中诱发炎症反应。活性氧 (ROS) 的积累是 BBP 毒性的主要表现，并伴随着抗氧化和解毒酶活性的变化。值得注意的是，促凋亡基因（p53和caspase-3）在第 28 天在 50 μg/L 和 500 μg/L 处理组中仍然显着上调。此外，BBP 通过与凋亡蛋白（P53 和 Caspase-3）形成稳定的复合物来干扰细胞凋亡。我们的研究结果有助于理解 BBP 的毒性机制，进一步促进 BBP 潜在环境风险的评估。