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环境科学学报（英文版）
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2026年10期
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Early-life exposure to flusilazole causes transgenerational cardiac developmental defects in zebrafish and its potential causes
Early-life exposure to flusilazole causes transgenerational cardiac developmental defects in zebrafish and its potential causes
摘要
With the growing use of novel triazole fungicides,concerns over their toxicity and ecological effects have in-tensified.This study investigated the transgenerational cardiac toxicity of flusilazole(FLU)in zebrafish embryos and its underlying mechanisms.Fertilized eggs were exposed to 0.5,1,or 2 pmol/L FLU,and larvae were reared in FLU-containing water until adulthood.These adults were then mated with unexposed fish to produce the F1 generation.The results showed that both FO and F1 larvae developed cardiac arrhythmia and exhibited increased blood flow.Transcriptome profiling of FO juveniles revealed significant enrichment in pathways governing car-diomyocyte development,differentiation,and apoptosis.In the hearts of both adult generations,the key car-diac function-related genes(nkx2.5,fli1,atp2al1,and atp2a2a)were upregulated,along with genes involved in cardiac development and calcium homeostasis,indicating impaired heart development.Importantly,cellular staining demonstrated that the decline in cardiac function was closely associated with enhanced apoptosis of cardiomyocytes.Furthermore,hereditary factors were shown to significantly contribute to the cardiac defects across generations.Overall,this study provides new mechanistic insights into pesticide-induced congenital heart disease,highlighting the role of apoptosis and gene dysregulation in transgenerational cardiac toxicity.
年，卷(期)：
2026, 168(10)
机标分类号：
TP311
H310.1
R392.11
在线出版日期：
2026年10月9日
