长期双A诱导的神经毒性:暴露风险,鱼中的分子命运及其潜在的植物修复
Rabia Tahir1, Samra2, Fozia Afzal3
1College of Animal Science and Technology, Sichuan Agricultural University, Chengdu, Sichuan 611130, China; Department of Zoology, The Islamia University of Bahawalpur, Bahawalpur, Punjab 63100, Pakistan.
The Science of the total environment
|September 7, 2024
概括
这项研究表明,双A (BPA) 通过损伤大脑和破坏神经功能,导致常见鱼的神经毒性. 石榴皮提取物有效抵消了BPA的作用.
科学领域:
- 环境毒理学环境毒理学
- 水生物质毒理学研究
- 鱼类生理学 鱼类生理学
背景情况:
- 双A (BPA) 是一种因其在塑料中广泛使用而在环境中普遍存在的内分泌干扰化学物质.
- 常见的鱼 (Cyprinus carpio) 是一种被广泛消费的鱼类物种,这使得它们成为评估饮食暴露风险的相关模型.
- 了解BPA在鱼类中的神经毒性作用和分子机制对于环境和食品安全至关重要.
研究的目的:
- 为了研究 Bisphenol A (BPA) 对常见鱼 (Cyprinus carpio) 的神经毒性作用.
- 阐明BPA诱导的神经毒性背后的分子机制,包括氧化应激,血脑屏障完整性和亡.
- 评估石榴皮 (PP) 对鱼类BPA诱导的神经毒性的潜在保护作用.
主要方法:
- 常见的鱼被暴露在BPA的次致命度 (96小时LC50的1/5) 六周.
- 进行了生物化学测试,以评估抗氧化酶活性 (CAT,SOD,GSH) 和脂质过氧化 (MDA,8-OHDG).
- 对紧结蛋白的基因表达分析,乙胆酶活性和亡标记物 (bcl-2,caspase,p53家族) 的基因表达分析进行了评估. 在一些组中,石榴皮与BPA联合使用.
主要成果:
- 暴露于BPA导致鱼大脑发生显著的氧化损伤,这表明抗氧化能力降低和脂质过氧化增加.
- 观察到功能性神经毒性,包括血脑屏障的破坏 (低调紧接口基因) 和神经传导障碍 (降低乙胆酶活性).
- 细胞死亡途径被BPA激活,这是关键调节基因的改变所证明的.
- 用8%粉末石榴皮 (PP) 作为食补充剂显著减轻了BPA诱导的神经毒性,将生物化学和分子标志物恢复到接近正常水平.
结论:
- 双A (BPA) 通过氧化应激,血脑屏障破坏和亡诱导普通鱼显著的神经毒性.
- 石榴皮 (PP) 显示出对鱼类BPA诱导的神经毒性的强烈保护作用.
- 用石榴皮丰富饮食可能是减轻BPA污染在食用鱼类中的不良影响的可行策略.
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