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The potential relationship between neurobehavioral toxicity and visual dysfunction of BDE-209 on zebrafish larvae: a pilot study

机译:BDE-209对斑马鱼幼虫的神经致毒性与视觉功能障碍的潜在关系:试验研究

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Background Although listed in the Stockholm Convention, commercial Decabromodiphenyl ether (c-DecaBDE) is still being produced in many factories and used as a kind of flame retardants primarily in plastic polymers and textiles. Widespread use offered many exposure ways of its major ingredient, BDE-209, to humans and the environment. Most current studies of BDE-209 focused on the health effects and toxicity of thyroid disruption, oxidative stress, neurotoxicity, and reproductive function, but seldom spread light on the relationship between neurobehavioral toxicity and visual dysfunction. Using zebrafish larvae model, we hope to uncover the potential relationship between the neurobehavioral and visual effects after exposure to BDE-209. Results BDE-209 exposure could not induce the changes of locomotion and path angle in 5?days post fertilization (dpf) larvae; however, 5?μg/L BDE-209 exposure caused locomotor hyperactivity and more responsive turns at 7 dpf. The social activity of 50?μg/L exposure group was significantly higher than the control group at 6 dpf. Besides, 5 and 50?μg/L exposure caused the upregulation and downregulation of four cone opsin genes, respectively. The expression of rhodopsin gene was not influenced by both concentration exposures. Conclusion The neurobehavioral effects induced by 5?μg/L BDE-209 exposure were consistent with the upregulation of four cone opsins in 7 dpf larvae. The low concentration of BDE-209 exposure caused the hyperactivity and more responsive turns of larvae possibly contributing to the disruption on the cone opsin expressions of larvae. Our results would provide the mechanism cue of neurobehavioral toxicity after BDE-209 exposure and call for more attention on the ecotoxicology studies of BDE-209.
机译:背景虽然斯德哥尔摩公约中列出,十溴二苯醚商业(商用十溴二苯醚)仍在许多工厂生产并用作主要在塑料聚合物和纺织品的一种阻燃剂。广泛使用提供了其主要成分,BDE-209的许多曝光的方式,对人体和环境。 BDE-209的目前大多数研究侧重于对健康的影响和破坏甲状腺,氧化应激,神经毒性和生殖功能的毒性,但很少波及神经行为毒性和视觉功能障碍之间的关系的光。使用斑马鱼模型,我们希望揭开神经行为和视觉效果之间的曝光后,BDE-209的潜在关系。结果BDE-209曝光不能诱导在5运动和路径的角度变化天后受精(dpf)的幼虫?;然而,5'微克/升BDE-209暴露引起运动活动过度和在7旦更具响应匝。 50?微克/升暴露组的社会活性比在6单丝旦对照组显著高。此外,图5和50?微克/升曝光分别引起的上调和四个锥形的下调视蛋白基因。视紫红质基因的表达不是由两个浓度暴露的影响。结论5?微克/升BDE-209暴露诱导的神经行为影响与四个锥体视蛋白在7旦幼虫的上调是一致的。 BDE-209曝光的低浓度导致多动症和幼虫更敏感的转向可能对锥体视蛋白幼虫表达的破坏贡献。 BDE-209曝光后我们的研究结果将提供神经行为毒性机制线索,并呼吁更多的注意力放在BDE-209的生态毒理学研究。

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