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滴滴涕对斑马鱼胚胎-幼鱼轴突生长、肌肉和运动行为的影响。

Effects of Dechlorane Plus exposure on axonal growth, musculature and motor behavior in embryo-larval zebrafish.

机构信息

State Key Laboratory of Marine Environmental Science of China (Xiamen University), College of the Environment and Ecology, Xiamen University, Xiamen 361102, PR China.

Institute of Environmental Safety and Human Health, Wenzhou Medical University, Wenzhou 325035, PR China.

出版信息

Environ Pollut. 2017 May;224:7-15. doi: 10.1016/j.envpol.2017.03.011. Epub 2017 Mar 10.

Abstract

Developmental neurobehavioral toxicity of Dechlorane Plus (DP) was investigated using the embryo-larval stages of zebrafish (Danio rerio). Normal fertilized embryos were waterborne exposed to DP at 15, 30, 60 μg/L beginning from 6 h post-fertilization (hpf). Larval teratology, motor activity, motoneuron axonal growth and muscle morphology were assessed at different developmental stages. Results showed that DP exposure significantly altered embryonic spontaneous movement, reduced touch-induced movement and free-swimming speed and decreased swimming speed of larvae in response to dark stimulation. These changes occurred at DP doses that resulted no significant teratogenesis in zebrafish. Interestingly, in accord with these behavioral anomalies, DP exposure significantly inhibited axonal growth of primary motoneuron and induced apoptotic cell death and lesions in the muscle fibers of zebrafish. Furthermore, DP exposure at 30 μg/L and 60 μg/L significantly increased reactive oxygen species (ROS) and malondialdehyde (MDA) formation, as well as the mRNA transcript levels of apoptosis-related genes bax and caspase-3. Together, our data indicate that DP induced neurobehavioral deficits may result from combined effects of altered neuronal connectivity and muscle injuries.

摘要

使用斑马鱼(Danio rerio)的胚胎-幼虫阶段研究了 Dechlorane Plus(DP)的发育神经行为毒性。从受精后 6 小时(hpf)开始,将正常受精的胚胎用水暴露于 15、30、60μg/L 的 DP 中。在不同的发育阶段评估了幼虫的畸形学、运动活动、运动神经元轴突生长和肌肉形态。结果表明,DP 暴露显著改变了胚胎的自发性运动,减少了触摸诱导的运动和自由游泳速度,并降低了幼虫对黑暗刺激的游泳速度。这些变化发生在 DP 剂量下,斑马鱼没有明显的致畸作用。有趣的是,与这些行为异常一致,DP 暴露显著抑制了初级运动神经元的轴突生长,并诱导了斑马鱼肌肉纤维的细胞凋亡和损伤。此外,DP 在 30μg/L 和 60μg/L 时显著增加了活性氧(ROS)和丙二醛(MDA)的形成,以及与细胞凋亡相关的 bax 和 caspase-3 基因的 mRNA 转录水平。总之,我们的数据表明,DP 诱导的神经行为缺陷可能是由于神经元连接改变和肌肉损伤的综合作用所致。

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