Metalaxyl is an acylanilide systemic fungicide that is widely applied and can readily enter ecosystems through leaching and soil runoff. This research utilized zebrafish as a model organism to thoroughly investigate the detrimental impacts of environmentally relevant levels of metalaxyl on the development of the notochord in zebrafish embryos and to elucidate the underlying molecular mechanisms through transcriptomics, pharmacological intervention and molecular biological detection. The preliminary results demonstrated that metalaxyl induced significant modifications in the developmental parameters of zebrafish embryos. This study has also assessed the long-term consequences of metalaxyl exposure during the embryonic development of zebrafish. This study have demonstrated that zebrafish exposed to metalaxyl exhibit a range of abnormalities, including defects in notochord vacuole biogenesis, somite segmentation disorders, anomalous notochord curvatures, craniofacial cartilage deformities, and irregular chordacentra mineralisation. Through transcriptomic and bioinformatics analysis, it was found that most of the genes exhibiting differential expression were linked to oxidative stress. Furthermore, the evidence indicated that oxidative stress was present, as demonstrated by increased malondialdehyde (MDA) production and a decrease in antioxidant enzyme activity (CAT, SOD, GSH). Interestingly, the developmental dysfunction induced by metalaxyl was partially rescued by chlorogenic acid. Overall, metalaxyl disrupts notochord and skeletal formation in zebrafish embryos by modulating oxidative stress mediated by reactive oxygen species.
Xiaofang Che,Yong Huang,Tianzhu Shen,Keyuan Zhong,You Wei,Guoqiang Fan,Kun Jia,Wei Yuan,Huiqiang Lu
Monosultap (Mon) is a broad-spectrum insecticide used in agricultural production to control stem borers in rice fields . Currently, little evidence shows how Mon affects notochord development in zebrafish ( Danio rerio ). In our study, zebrafish embryos were exposed to 0.25, 0.5, and 0.75 mg/L Mon to determine the effects of different concentrations of Mon on notochord development. Mon exposure reduced the body length, decreased the heart rate and hatchability, and induced notochord deformity in zebrafish. The effects of Mon exposure on the internal organization of the notochord and the structural abnormalities were determined based on histological staining of paraffinized tissue sections. Quantitative polymerase chain reaction (qPCR) and in situ hybridization findings revealed that the expression levels of genes related to notochord development ( shha, col2a, and ptch2 ) showed an increasing trend in a concentration-dependent manner. An abnormal increase of apoptosis and cell proliferation in some parts of the notochord suggested that Mon exposure could cause developmental abnormality of the notochord. This study revealed the toxicity of Mon in notochord development. Our findings provide information in assessing the risk of Mon to the ecological environment and human health.
危险品化学品经营许可证（带存储）