Broad applications and exposure to the fungicide maneb can lead to toxicity in non-target organisms. Maneb is also associated with neurogenerative diseases such as Parkinson's disease (PD). The objectives of this study were to determine the acute toxicity of maneb to zebrafish by measuring mitochondrial bioenergetics, locomotor activity, and the expression of genes related to the oxidative damage response, as well as those related to dopamine signaling due to its association with PD. Zebrafish embryos at 6 h post-fertilization (hpf) were exposed to either solvent control (0.1% DMSO, v/v), or one dose of 0.1, 0.5, 1.0 and 10.0 µM maneb for 96 h. Maneb was moderately toxic to zebrafish embryos, and had a 96-h LC₅₀ value of 4.29 μM (~ 1.14 mg/L). Maneb induced a dose-dependent increase in mortality, decreased hatching rate, and increased notochord deformity rate at both 1.0 and 10.0 µM after 72 and 96 h. Total body length was also significantly reduced with 1.0 µM maneb. A 50–60% decrease in mean basal oxygen consumption rate was also observed in embryos following a 24 hpf exposure to 10.0 µM maneb but oligomycin-induced ATP production and FCCP-induced maximum respiration remained unaffected. No change was detected in the expression levels of genes associated with oxidative stress (sod1 and sod2), nor those related to dopamine synthesis (th1), dopamine transporter (dat), dopamine receptors (drd1, drd2a, drd3, and drd4b). Thus, modifying the expression of these transcripts may not be a mechanism for maneb-induced developmental toxicity in zebrafish. To assess the potential for neurotoxicity, a dark photokinesis assay was conducted in larvae following 7 d exposure to 0.1, 0.5 and 1.0 μM maneb. Larvae exposed to 0.5 and 1.0 μM maneb showed signs related to hypoactivity, and this reduced activity is hypothesized to be associated with notochord defects as this deformity was prevalent at higher concentrations of maneb. Overall, these data demonstrate that maneb negatively affects embryonic development (i.e. notochord development), affects basal oxygen consumption rates of embryos, and induces hypoactivity in larval fish. This study improves understanding regarding the developmental neurotoxicity of the fungicide maneb to zebrafish.

广泛应用和暴露于杀真菌剂甲炔可导致非目标生物体中的毒性。Maneb还与神经生成性疾病（如帕金森氏病（PD））相关。这项研究的目的是通过测量线粒体的生物能，运动活性以及与氧化损伤反应有关的基因的表达，以及与多巴胺信号传导有关的基因（由于其与PD的关系）来确定maneb对斑马鱼的急性毒性。受精后6 h（hpf）的斑马鱼胚胎暴露于溶剂对照（0.1％DMSO，v / v）或一剂0.1、0.5、1.0和10.0 µM maneb的溶液中暴露96 h。Maneb对斑马鱼的胚胎具有中等毒性，并且具有96小时的LC ₅₀值为4.29μM（〜1.14 mg / L）。在72和96小时后，Maneb分别以1.0和10.0 µM引起死亡率的剂量依赖性增加，孵化率降低和脊索畸形率增加。用1.0 µM maneb还可显着减少总体长。在24 hpf暴露于10.0 µM maneb后，胚胎中的平均基础耗氧率也降低了50-60％，但寡聚霉素诱导的ATP产生和FCCP诱导的最大呼吸仍然不受影响。未检测到与氧化应激相关的基因（sod1和sod2）的基因表达水平变化，也未检测到与多巴胺合成（th1），多巴胺转运蛋白（dat），多巴胺受体（drd1，drd2a ）相关的基因的表达水平的变化。，drd3和drd4b）。因此，修饰这些转录本的表达可能不是斑马鱼中maneb诱导的发育毒性的机制。为了评估潜在的神经毒性，在暴露于0.1、0.5和1.0μMmaneb的7 d后，在幼​​虫中进行暗光动力学分析。幼虫暴露于0.5和1.0μMManeb时显示出与机能减退相关的征兆，据推测，这种降低的活性与脊索缺损有关，因为这种畸形在较高的maneb浓度下普遍存在。总体而言，这些数据表明，maneb会对胚胎发育（即脊索发育）产生负面影响，影响胚胎的基础耗氧率，并导致幼体鱼活动减退。这项研究提高了对杀菌剂maneb对斑马鱼的发育神经毒性的了解。