Abstract：
Tris (2-chloroethyl) phosphate (TCEP) is a crucial organophosphorus flame retardant widely used in many industrial and commercial products. Available reports reported that TCEP could cause various toxicological effects on organisms, including humans. Unfortunately, toxicity data for TCEP (particularly on neurotoxicity) on aquatic organisms are lacking. In the present study, Danio rerio were exposed to different concentrations of TCEP for 42 days (chronic exposure), and oxidative stress, neurotoxicity, sodium, potassium-adenosine triphosphatase (Na+, K+-ATPase) activity, and histopathological changes were evaluated in the brain. The results showed that TCEP (100 and 1500 µg L-1) induced oxidative stress and significantly decreased the activities of antioxidant enzymes (SOD, CAT and GR) in the brain tissue of zebrafish. In contrast, the lipid peroxidation (LPO) level was increased compared to the control group. Exposure to TCEP inhibited the acetylcholinesterase (AChE) and Na+,K+-ATPase activities in the brain tissue. Brain histopathology after 42 days of exposure to TCEP showed cytoplasmic vacuolation, inflammatory cell infiltration, degenerated neurons, degenerated purkinje cells and binucleate. Furthermore, TCEP exposure leads to significant changes in dopamine and 5-HT levels in the brain of zebrafish. The data in the present study suggest that high concentrations of TCEP might affect the fish by altering oxidative balance and inducing marked pathological changes in the brain of zebrafish. These findings indicate that chronic exposure to TCEP may cause a neurotoxic effect in zebrafish.
摘要：
磷酸三（2-氯乙基）酯（TCEP）是一种重要的有机磷阻燃剂，广泛用于许多工业和商业产品中。现有报告报告称，TCEP可能对生物体造成各种毒理学影响，包括人类。不幸的是,缺乏TCEP对水生生物的毒性数据（特别是神经毒性）。在本研究中,Daniorerio暴露于不同浓度的TCEP42天（慢性暴露），和氧化应激，神经毒性，钠,钾-腺苷三磷酸酶（Na+，K+-ATP酶）活性，并评估了大脑的组织病理学变化。结果表明，TCEP（100和1500µgL-1）诱导氧化应激并显着降低抗氧化酶（SOD，斑马鱼脑组织中的CAT和GR）。相比之下,与对照组相比，脂质过氧化（LPO）水平升高。暴露于TCEP抑制乙酰胆碱酯酶（AChE）和Na+，脑组织中的K+-ATP酶活性。暴露于TCEP42天后的脑组织病理学显示细胞质空泡化，炎性细胞浸润，退化的神经元，退化的浦肯野细胞和双核。此外，TCEP暴露会导致斑马鱼大脑中多巴胺和5-HT水平的显着变化。本研究的数据表明，高浓度的TCEP可能通过改变斑马鱼大脑的氧化平衡和诱导明显的病理变化来影响鱼类。这些发现表明，长期暴露于TCEP可能会在斑马鱼中引起神经毒性作用。
