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Aquat Toxicol

Title:		Spiromesifen conferred abnormal development in zebrafish embryos by inducing embryonic cytotoxicity via causing oxidative stress
Author(s):		Wang M; Wang H; Chen G; Liu J; Hu T;
Address:		"Key Laboratory of Biorheological Science and Technology (Chongqing University), Ministry of Education, State and Local Joint Engineering Laboratory for Vascular Implants, No. 174, Shazheng, Street, Shapingba District, Bioengineering College of Chongqing University, Chongqing 400030, PR China. Key Laboratory of Biorheological Science and Technology (Chongqing University), Ministry of Education, State and Local Joint Engineering Laboratory for Vascular Implants, No. 174, Shazheng, Street, Shapingba District, Bioengineering College of Chongqing University, Chongqing 400030, PR China. Electronic address: tzhu@cqu.edu.cn"
Journal Title:		Aquat Toxicol
Year:		2022
Volume:		20221012
Issue:
Page Number:		106324 -
DOI:		10.1016/j.aquatox.2022.106324
ISSN/ISBN:		1879-1514 (Electronic) 0166-445X (Linking)
Abstract:		"Spiromesifen (SPF) is widely used in agriculture to protect against herbivorous mites, whose residues may be harmful to the environment. However, the toxicity assessment of SPF is insufficient. Here, we investigated the toxicological effects of SPF using zebrafish embryos as an animal model. The results showed that SPF exposure solutions at 10, 20, 30, and 40 muM caused cytotoxicity in zebrafish embryos such as reactive oxygen species (ROS) accumulation, mitochondrial membrane potential decrease, cell division arrest, and apoptosis, which further led to developmental toxicity in zebrafish embryos including delayed hatching, decreased survival rate and spontaneous curling rate, and severe morphological deformities. SPF also induced apoptosis via changes in the expressions of apoptosis-related marker genes, caused immunotoxicity by reducing the number of macrophages and the activity of AKP/ALP and increasing inflammatory factors, and disturbed endogenous antioxidant systems via changes SOD, CAT, and GST activities as well as MDA and GSH contents. Therefore, the potential mechanism that caused embryonic developmental toxicity appeared to be related to the generation of oxidative stress by an elevation in ROS and changes in apoptosis-, immune-, antioxidant-related markers. The antioxidant system and inflammatory response simultaneously participated in and resisted the threat of SPF to prevent tissue damage. Taken together, spiromesifen induced oxidative stress to contribute to developmental toxicity in zebrafish embryos by inducing embryonic cytotoxicity. Our study provides new insight into the toxicity assessment of SPF to non-target organisms"
Keywords:		"Animals *Zebrafish/metabolism Reactive Oxygen Species/metabolism Antioxidants/metabolism Embryo, Nonmammalian *Water Pollutants, Chemical/toxicity Oxidative Stress Embryonic Development Apoptosis Superoxide Dismutase/metabolism Cytotoxicity Developmental;"
Notes:		"MedlineWang, Mingxing Wang, Huiyun Chen, Guoliang Liu, Juan Hu, Tingzhang eng Netherlands 2022/10/17 Aquat Toxicol. 2022 Nov; 252:106324. doi: 10.1016/j.aquatox.2022.106324. Epub 2022 Oct 12"