Effects of haloxyfop-p-methyl on the developmental toxicity, neurotoxicity, and immunotoxicity in zebrafish

Pesticides are extensively used in agricultural production, and their residues in soil, water, and agricultural products have become a threat to aquatic ecosystem. In this study, the toxicity of haloxyfop-p-methyl, an ary-loxyphenoxypropionate herbicide was studied using the model animal zebrafish. The development of zebrafish larvae was affected by haloxyfop-p-methyl including spinal deformities, decreased body length, slow heart rate, and large yolk sac area. Behavior analysis revealed that behavior activity of larvae was weakened significantly including shortened displacement distance, reduced swimming speed, increased angular speed winding degrees, in accordance with higher AChE activity. Besides, exposure to haloxyfop-p-methyl could induce oxidative stress companied by the increased intents of ROS, MDA and increased activities of CAT and SOD. In immunotoxicity, haloxyfop-p-methyl not only reduced the innate immune cells such as neutrophils and macrophages, but also affected T cells mature in thymus. Furthermore, haloxyfop-p-methyl could induce neutrophils apoptosis, accompanied with the upregulation of the expression of proapoptotic protein such as Bax and P53 and the downregulation of the expression of antiapoptotic protein Bcl-2. In addition, haloxyfop-p-methyl could induce the expression of Jak, STAT and proinflammatory cytokine genes (IFN-gamma , TNF-alpha , and IL-8). These results indicate that haloxyfop-p-methyl induces developmental toxicity, neurotoxicity, and immunotoxicity in zebrafish, providing a perspective on the toxicological mechanism of haloxyfop-p-methyl in teleosts.

Automated summary

Pesticides, such as haloxyfop-p-methyl, are harmful to the aquatic ecosystem as they leave residues in soil, water, and agricultural products. This study investigated the toxic effects of haloxyfop-p-methyl on zebrafish and found developmental, neurotoxic, and immunotoxic effects. Zebrafish larvae exhibited spinal deformities, decreased body length, slow heart rate, and enlarged yolk sac area. Behavior analysis showed reduced activity, accompanied by higher AChE activity. Exposure to haloxyfop-p-methyl also induced oxidative stress and affected immune cell populations in the thymus. Furthermore, haloxyfop-p-methyl caused neutrophil apoptosis and increased expression of proinflammatory cytokine genes. These findings provide insights into the toxicological mechanisms of haloxyfop-p-methyl in teleosts.