アンチモンによるゼブラフィッシュ（Danio rerio）における造血障害に対する慢性低濃度曝露のメカニズム的洞察を提供する単一細胞トランスクリプトミクスベースの分析

Antimony (Sb), a widely used strategic metal, has raised growing concerns due to its environmental persistence and potential toxicity. However, the chronic effects of low-level Sb exposure on hematopoietic function remain poorly understood. In this study, zebrafish (Danio rerio) were exposed to Sb at concentrations of 0, 5, 50, 500, and 5000 μg/L for 28 days to investigate the hematotoxic effects and underlying mechanisms. Biochemical assays revealed that Sb exposure significantly disrupted blood glucose and lipid metabolism, reduced glucose levels, and altered lipid profiles in a concentration-dependent manner. In addition, Sb exposure increased cytokines such as NFAT, M-CSF, and IL-11. Histopathology revealed pronounced damage to the kidney, the primary hematopoietic organ in zebrafish. Single-cell RNA sequencing identified 13 hematopoietic cell populations. Differentially expressed genes were significantly enriched in the IL-17 pathway, with downstream activation of NF-κB and increased expression of TNF-α and MMP-9. These findings provide mechanistic insights into Sb-induced hematopoietic imbalance and renal injury, highlighting the role of IL-17-mediated inflammatory responses in mediating Sb toxicity. Overall, this study offers a valuable reference for ecological risk assessment and health hazard evaluation of Sb contamination.