4.7 Article

Effect of monosultap on notochord development in zebrafish (Danio rerio) embryos

期刊

TOXICOLOGY
卷 477, 期 -, 页码 -

出版社

ELSEVIER IRELAND LTD
DOI: 10.1016/j.tox.2022.153276

关键词

Monosultap; Notochord distortion; Vacuole collapse; Apoptosis; Oxidative stress

资金

  1. National Natural Science Foundation of China [32170853]
  2. National Key R&D Program of China [2018YFA0801000]
  3. Natural Science Foundation of Jiangxi Province, China [20212ACB205007]
  4. Science and Technology Foundation of the Education Department of Jiangxi Province, China [GJJ201002, GJJ211441]
  5. Ganzhou Science and technology innovation project, China [202101094931, 202060]
  6. Open Research Fund Program of Jiangxi Provincal Key Laboratory of Low-Carbon Solid Waste Recycling (Gannan Normal University), China [20212BCD42015]

向作者/读者索取更多资源

This study revealed the toxicity of Mon in notochord development in zebrafish. Mon exposure led to reduced body length, decreased heart rate and hatchability, and induced notochord deformity. Histological staining and molecular biology experiments showed that Mon exposure also affected the internal structure and gene expression levels of the notochord. Therefore, this research suggests that the use of Mon may pose risks to the ecological environment and human health.
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.

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