Jin Yuanxiang, Liu Zhenzhen, Peng Tao, Fu Zhengwei
College of Biological and Environmental Engineering, Zhejiang University of Technology, Hangzhou 310032, China.
College of Biological and Environmental Engineering, Zhejiang University of Technology, Hangzhou 310032, China.
Fish Shellfish Immunol. 2015 Apr;43(2):405-14. doi: 10.1016/j.fsi.2015.01.010. Epub 2015 Jan 26.
Chlorpyrifos (CPF) is one of the most toxic pesticides in aquatic ecosystem, but its toxicity mechanisms to fish are still not fully understood. This study examined the toxicity targets of CPF in early life stage of zebrafish on the endpoints at developmental toxicity, neurotoxicity, oxidative stress and immunotoxicity. Firstly, CPF exposure decreased the body length, inhibited the hatchability and heart rate, and resulted in a number of morphological abnormalities, primarily spinal deformities (SD) and pericardial edema (PE), in larval zebrafish. Secondly, the free swimming activities and the swimming behaviors of the larvae in response to the stimulation of light-to-dark photoperiod transition were significantly influenced by the exposure to 100 and 300 μg/L CPF. In addition, the activity of acetylcholinesterase (AChE) and the transcription of some genes related to neurotoxicity were also influenced by CPF exposure. Thirdly, CPF exposure induced oxidative stress in the larval zebrafish. The malondialdehyde (MDA) levels increased and the glutathione (GSH) contents decreased significantly in a concentration-dependent manner after the exposure to CPF for 96 hours post fertilization (hpf). CPF affected not only the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX) and glutathione S-transferase (GST), but also the transcriptional levels of their respective genes. Finally, the mRNA levels of the main cytokines including tumor necrosis factor α (Tnfα), interferon (Ifn), interleukin-1 beta (Il-1β), interleukin 6 (Il6), complement factor 4 (C4) in the larvae increased significantly after the exposure to 100 or 300 μg/L CPF for 96 hpf, suggesting that the innate immune system disturbed by CPF in larvae. Taken together, our results suggested that CPF had the potential to cause developmental toxicity, behavior alterations, oxidative stress and immunotoxicity in the larval zebrafish.
毒死蜱（CPF）是水生生态系统中毒性最强的农药之一，但其对鱼类的毒性机制仍未完全明确。本研究从发育毒性、神经毒性、氧化应激和免疫毒性等方面，探究了CPF在斑马鱼幼鱼早期生活阶段的毒性靶点。首先，暴露于CPF会使斑马鱼幼鱼体长缩短，抑制孵化率和心率，并导致多种形态异常，主要为脊柱畸形（SD）和心包水肿（PE）。其次，暴露于100和300μg/L的CPF会显著影响幼鱼的自由游泳活动以及对光暗周期转换刺激的游泳行为。此外，CPF暴露还会影响乙酰胆碱酯酶（AChE）的活性以及一些与神经毒性相关基因的转录。第三，CPF暴露会诱导斑马鱼幼鱼产生氧化应激。受精后96小时（hpf）暴露于CPF后，丙二醛（MDA）水平升高，谷胱甘肽（GSH）含量显著下降，且呈浓度依赖性。CPF不仅影响超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、谷胱甘肽过氧化物酶（GPX）和谷胱甘肽S-转移酶（GST）的活性，还影响其各自基因的转录水平。最后，暴露于100或300μg/L的CPF 96 hpf后，幼鱼体内包括肿瘤坏死因子α（Tnfα）、干扰素（Ifn）、白细胞介素-1β（Il-1β）、白细胞介素6（Il6）、补体因子4（C4）在内的主要细胞因子的mRNA水平显著升高，表明CPF扰乱了幼鱼的先天免疫系统。综上所述，我们的结果表明CPF有可能对斑马鱼幼鱼造成发育毒性、行为改变、氧化应激和免疫毒性。
