Di (2-ethylhexyl) phthalate (DEHP) is a widely used plasticizer, also known as a developmental toxicant, but its neurobehavioral toxicity remains elusive. This study evaluated the neurobehavioral toxicity and its possible mechanism in larval zebrafish. Embryos at gastrula period (~6 h post fertilization, hpf) were exposure to DEHP (0, 1, 2.5, 5 and 10 mg/L) for 7 days. Spontaneous tail movement in embryos and swimming activity in larvae were monitored. Alterations in the mRNA expression of genes involved in dopamine signaling and apoptosis pathway were assessed. In situ apoptotic cells were assessed by Acridine orange staining, and oxidative damage were measured using enzymatic assay. The behavior results showed that DEHP inhibited spontaneous tail movement and decreased locomotor activities in the light/dark behavioral test. Meanwhile, behavioral changes were accompanied by increased apoptosis and malondialdehyde (MDA) content, decreased superoxide dismutase (SOD) activity and dopamine (DA) content, and perturbed the expression of genes associated with the synthesis (th), reuptake (dat) and metabolism (mao) of DA, with dopamine receptors (DRs), and with the apoptosis pathway (p53, bax, bcl2, caspase-3, caspase-8, caspase-9). The findings will help to illuminate the possible neurobehavioral toxicity mechanisms of organism exposure to DEHP.

邻苯二甲酸二 (2-乙基己基)酯 (DEHP) 是一种广泛使用的增塑剂，也被称为发育毒物，但其神经行为毒性仍然难以捉摸。本研究评估了斑马鱼幼虫的神经行为毒性及其可能的机制。原肠胚期（受精后约 6 小时，hpf）胚胎暴露于 DEHP（0、1、2.5、5 和 10 毫克/升）7 天。监测胚胎中的自发尾巴运动和幼虫的游泳活动。评估了参与多巴胺信号传导和细胞凋亡途径的基因的 mRNA 表达变化。通过吖啶橙染色评估原位凋亡细胞，并使用酶测定法测量氧化损伤。行为结果表明，DEHP 在光/暗行为测试中抑制了自发的尾巴运动并降低了运动活动。同时，th )、DA 的再摄取 ( dat ) 和代谢 ( mao )，与多巴胺受体 (DRs) 和凋亡途径 ( p53、bax、bcl2、caspase-3、caspase-8、caspase-9 ) 相关。这些发现将有助于阐明有机体暴露于 DEHP 的可能的神经行为毒性机制。