TPT disrupts early embryonic development and glucose metabolism of marine medaka in different salinites

Triphenyltin (TPT) is an organotin compound frequently detected in coastal estuaries, yet studies on TPT's effects in regions with significant salinity fluctuations, such as coastal estuaries, are currently limited. To investigate the toxic effects of TPT under different salinity conditions, this study focused on marine medaka (Oryzias melastigma) embryos. Through early morphological observations, RNA-seq analysis, biochemical marker assays, and qPCR detection, we explored the impact of TPT exposure on the early embryonic development of marine medaka under varying salinities. The study found that TPT exposure significantly increased embryo mortality at salinities of 0 ppt and 30 ppt. RNA-seq analysis revealed that TPT primarily affects glucose metabolism and glycogen synthesis processes in embryos. Under high salinity conditions, TPT may inhibit glucose metabolism by suppressing glycolysis and promoting gluconeogenesis. Furthermore, TPT exposure under different salinities led to the downregulation of genes associated with the insulin signaling pathway (ins, insra, irs2b, pik3ca, pdk1b, akt1, foxo1a), which may be linked to suppressed glucose metabolism and increased embryonic mortality. In summary, TPT exposure under different salinities affects the early development of marine medaka embryos and inhibits glucose metabolism. This study provides additional data to support research on organotin compounds in coastal estuaries.