当前位置: X-MOL 学术Chem. Biol. Interact. › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Bromoacetic acid induces neurogenic injury in the chicken brain by activating oxidative stress and NF-κB inflammatory pathway
Chemico-Biological Interactions ( IF 4.7 ) Pub Date : 2022-08-18 , DOI: 10.1016/j.cbi.2022.110115
Jiwen Liu 1 , Yuting Wu 1 , Shuhui Liu 1 , Zhangshan Gao 1 , Wentao Fan 1 , Chenchen Ding 1 , Zhihui Tang 1 , Shuo Zhang 1 , Xizhi Shi 2 , Lei Tan 3 , Yan Luo 3 , Suquan Song 1
Affiliation  

The bromoacetic acid (BAA) is one of the most teratogenic and neurotoxic disinfection byproducts. Birds take environmental water as their habitat and are inevitably affected by BAA in the environment. However, the neurotoxicity caused by BAA in birds has not been reported and the mechanism remains unclear. In this study, we chose chickens as the avian model to explore the effects of different concentrations of BAA on the brain tissues. Here, we selected the 3 μg/L dose of BAA detected in Tai Lake basin as a reference, and designed 1-, 100-, and 1000-fold of the environmental exposure dose as the experimental doses to explore the neurotoxicity of BAA in birds. Results showed that BAA increased the number of pyknotic nuclear neurons, deformed vascular sheaths, and glial cells in the brain. BAA inhibited the activity of antioxidant enzymes and the expression of antioxidant genes. With the increase of BAA concentration, the oxidative stress-responsive transcription factor NF-κB was activated. Furthermore, BAA remarkably changed the expression of lipid metabolism related genes (i.e., acc, gpat, hmgr, pparα, cpt1, and ampkα). Importantly, BAA decreased the mRNA and protein expression levels of autophagy-related genes (i.e., atg5, ulk1, beclin1, and lc3). Meantime, BAA increased the mRNA and protein levels of apoptotic and pro-apoptotic genes, such as p53, bax, cytochrome c, caspase-9, and caspase-3. Overall, our study provided new insights into the potential neurotoxic effects of BAA in birds, which was important for the clinical monitoring and prevention of BAA.



中文翻译:

溴乙酸通过激活氧化应激和NF-κB炎症通路诱导鸡脑神经源性损伤

溴乙酸 (BAA) 是最具致畸性和神经毒性的消毒副产物之一. 鸟类以环境水为栖息地,不可避免地受到环境中BAA的影响。然而,BAA对鸟类的神经毒性尚未见报道,其机制尚不清楚。在本研究中,我们选择鸡作为鸟类模型来探索不同浓度 BAA 对脑组织的影响。在此,我们选取​​太湖流域检测到的 3 μg/L 剂量的 BAA 作为参考,设计了 1、100 和 1000 倍的环境暴露剂量作为实验剂量,探索 BAA 在鸟类中的神经毒性。 . 结果表明,BAA 增加了大脑中固缩核神经元、变形的血管鞘和神经胶质细胞的数量。BAA抑制抗氧化酶的活性和抗氧化基因的表达。随着 BAA 浓度的增加,氧化应激反应转录因子NF-κB被激活。此外,BAA 显着改变了脂质代谢相关基因(即acc gpat hmgr pparα cpt1ampkα)。重要的是,BAA 降低了自噬相关基因(即atg5 ulk1 beclin1lc3)的 mRNA 和蛋白质表达水平。同时,BAA 增加了凋亡和促凋亡基因的 mRNA 和蛋白质水平,例如p53 bax细胞色素c caspase-9caspase-3. 总体而言,我们的研究为 BAA 在鸟类中的潜在神经毒性作用提供了新的见解,这对于 BAA 的临床监测和预防非常重要。

更新日期:2022-08-21
down
wechat
bug