Work

Triphenyltin chloride induces hepatic toxicity in zebrafish by disrupting lipid metabolism and cell fate: involvement of MAPK/ERK signaling

Year: 2026

Type: article

Abstract: Triphenyltin chloride (TPTC) is widely used as a fungicide and marine antifouling compound, and its environmental persistence raises concerns regarding aquatic toxicity. In this study, zebrafish (Danio rerio) larvae at 72 hours post-fertilization (hpf) were exposed to TPTC at concentrations of 5, 10, and 15 μg/L until 144 hpf. Using fluorescence microscopy, Oil Red O staining, hematoxylin-eosin (H&E) staining, enzyme activity assays, and quantitative real-time PCR (qPCR), we evaluated hepatic morphology, lipid metabolism, hepatocyte proliferation, apoptosis, and MAPK/ERK signaling-related transcriptional responses. The results showed that TPTC exposure induced lipid metabolism disorder and subsequent lipid accumulation in the liver. In addition, TPTC exposure inhibited hepatocyte proliferation while promoting apoptosis. Meanwhile, increased expression of MAPK/ERK signaling-related genes was observed in the exposure groups. Notably, pharmacological inhibition of MEK by PD98059 partially alleviated TPTC-induced hepatic abnormalities, suggesting the involvement of MAPK/ERK signaling in TPTC-mediated hepatotoxicity. In conclusion, TPTC triggers hepatic steatosis and imbalance of cell fate in zebrafish, with MAPK/ERK signaling responses potentially contributing to these toxic effects. This study provides new insights into the toxicological effects of organotin compounds in aquatic organisms and contributes to environmental risk assessment of TPTC.

Source: Journal of Hazardous Materials Advances

DOI: 10.1016/j.hazadv.2026.101516