The effect of combined exposure to decabromodiphenyl ether (BDE-209) and lead (Pb) on neurodevelopment of zebrafish (Danio rerio) larvae was investigated. Zebrafish embryos were exposed to Pb (0, 5, 10, 20 µg/L) and BDE-209 (0, 50, 100, 200 µg/L), either alone or in combination (Mix1: 5 + 50 µg/L, Mix2: 10 + 100 µg/L, Mix3: 20 + 200 µg/L) for up to 144 h post-fertilization. Growth of secondary motoneuron axons and expression of genes related to central nervous system development was significantly inhibited in Mix3 co-exposure group. A significant increase in reactive oxygen species (ROS), lipid peroxidation, DNA damage, and perturbation of the antioxidant system was detected in the Mix3 group compared to single-toxicant treatments or control. Depressed locomotor activity was recorded in the Mix2 and Mix3 groups. Addition of N-acetyl cysteine to Mix3 eliminated excessive ROS, and protected against lipid peroxidation, DNA damage, and locomotor dysfunction. Pb uptake was increased in the presence of BDE-209, but BDE-209 bioconcentration and the ability to metabolize BDE-209 were decreased in the presence of Pb. These results suggest that BDE-209 and Pb have a synergistic disruptive effect on neurodevelopment in zebrafish larvae by enhanced generation of ROS, which is a major factor that contributes to developmental neurotoxicity.

中文翻译：

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铅和十溴二苯醚联合接触对斑马鱼幼虫神经发育的影响。

研究了十溴二苯醚（BDE-209）和铅（Pb）联合暴露对斑马鱼（Danio rerio）幼虫神经发育的影响。斑马鱼胚胎单独或组合（混合1：5 + 50 µg / L，分别暴露于Pb（0、5、10、20 µg / L）和BDE-209（0、50、100、200 µg / L）中暴露，受精后最多144小时，混合2：10 + 100 µg / L，混合3：20 + 200 µg / L）。在Mix3共暴露组中，继发运动神经元轴突的生长和与中枢神经系统发育相关的基因的表达受到显着抑制。与单一毒物治疗或对照相比，在Mix3组中发现了活性氧（ROS），脂质过氧化，DNA损伤和抗氧化剂系统扰动的显着增加。在Mix2和Mix3组中记录到运动能力下降。向Mix3中添加N-乙酰半胱氨酸可消除过量的ROS，并防止脂质过氧化，DNA损伤和运动功能障碍。在存在BDE-209的情况下，Pb的吸收增加，但是在存在Pb的情况下，BDE-209的生物浓度和代谢BDE-209的能力降低。这些结果表明，BDE-209和Pb通过增强ROS的生成对斑马鱼幼虫的神经发育具有协同破坏作用，这是导致发育性神经毒性的主要因素。