Department of Pathology, Faculty of Veterinary, Atatürk University, TR-25240, Erzurum, Turkey.
Department of Aquaculture, Faculty of Fisheries, Atatürk University, TR-25240, Erzurum, Turkey; Faculty of Fisheries, Aquatic Biotechnology Laboratory, Atatürk University Erzurum, TR-25240, Turkey.
Neurotoxicology. 2018 Dec;69:60-67. doi: 10.1016/j.neuro.2018.09.003. Epub 2018 Sep 14.
In this study, we investigated the potential neuro-toxicological mechanism of the glufosinate in the brain of zebrafish larvae in terms of BDNF and c-Fos proteins by evaluating apoptosis, immunofluorescence BDNF, and c-FOS activation. We also measured survival rate, hatching rate, and body malformations during 96 h exposure time. For this purpose, zebrafish embryos were treated with graded concentrations of dosing solutions (0.5, 1, 3, and 5 ppm) of glufosinate. End of the treatment, acridine orange staining was used to detect apoptotic cells in the brain of zebrafish larvae at 96 hpf. Texas Red and FITC/GFP labeled protein-specific antibodies were used in immunofluorescence assay for BDNF and c-FOS, respectively. The results have indicated that exposure to glufosinate caused to embryonic death, hatching delay, induction of apoptosis, increasing of c-FOS activity and the level of BDNF in a dose-dependent manner. As a conclusion, we suggested that c-Fos might play a role in the regulation of BDNF which responses to prevent the cell from apoptosis even in case of unsuccessful in zebrafish larvae exposed to glufosinate.
在这项研究中，我们通过评估细胞凋亡、免疫荧光 BDNF 和 c-FOS 激活，研究了草甘膦在斑马鱼幼虫大脑中的潜在神经毒性机制，涉及到 BDNF 和 c-Fos 蛋白。我们还在 96 小时暴露时间内测量了存活率、孵化率和身体畸形。为此，用不同浓度（0.5、1、3 和 5ppm）的草甘膦处理斑马鱼胚胎。在 96 hpf 时，用吖啶橙染色检测斑马鱼幼虫大脑中的凋亡细胞。用 Texas Red 和 FITC/GFP 标记的蛋白特异性抗体分别进行 BDNF 和 c-FOS 的免疫荧光测定。结果表明，草甘膦暴露会导致胚胎死亡、孵化延迟、凋亡诱导、c-FOS 活性增加和 BDNF 水平呈剂量依赖性增加。总之，我们认为 c-Fos 可能在 BDNF 的调节中发挥作用，即使在斑马鱼幼虫暴露于草甘膦的情况下，这种调节也可以防止细胞凋亡。
