Tengzhou Li,Luoxin Li,Bin Liu,Shaoying Xing,Ling Liu,Ping Li,Zhi-Hua Li
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.
Triphenyltin (TPT), a widely used environmental contaminant in antifouling paints, is known for its neurotoxic effects. To investigate the multigenerational impacts of long-term exposure (6 weeks) to environmental concentrations of TPT (100 ng/L) on either parent, we performed mixed mating between control and exposed groups (males or females). Although there was no direct contact with TPT in the subsequent generations, both the first and second generations displayed behavioral abnormalities, including reduced activity and impaired cognitive function, with pronounced gender differences and anxiety-like behaviors. Females were more susceptible than males, displaying a significantly increased time spent in the mirror-proximal zone in both F1 and F2 generations. Additionally, F0 females exhibited a marked reduction in the time spent in the bright area, further supporting the role of sex differences in behavioral responses. Notably, the maternal contribution of marine medaka ( Oryzias melastigma ) played a more significant role in the inheritance of TPT-induced cognitive deficits. A reduction in DA levels and AChE activity was observed across generations, regardless of gender, underscoring the critical role of DA-AChE balance in maintaining cognitive function. Additionally, gender differences and the hereditary effects of TPT exposure on anxiety-like behaviors were strongly associated with the transcriptional regulation of pparγ and gst . Impaired transcription of key genes in the dopaminergic system resulted in reduced DA levels, with the intergenerational transmission of mao being closely linked to behavioral impairments. In summary, TPT-induced neurotoxicity presents both hereditary effects and gender-specific differences, emphasizing the maternal influence in the inheritance of cognitive abilities and shedding light on the genetic impact of parental exposure.
Sediments function as a secondary and significant source of tributyltin (TBT) and triphenyltin (TPT) in aquatic ecosystems and may pose a potential threat on benthic organisms and human health. The subchronic toxicity of sediment-associated TBT or TPT to snails Bellamya aeruginosa at environmentally relevant concentrations was investigated in this study. Multiple endpoints at the biochemical [ethoxyresorufin-O-deethylase (EROD), superoxide dismutase (SOD), catalase (CAT), protein carbonyl content (PCC) and lipid peroxidation (LPO)] and transcriptomic levels were examined.TBT or TPT in sediment could induce antioxidant enzymes’ activities and result in oxidative damage in the hepatopancreas of B. aeruginosa after 28-day exposure. A transcriptomic profile of B. aeruginosa exposed to TBT and TPT was reported. CYP genes and EROD activity were sensible and reliable biomarkers for toxicity assessment of TBT or TPT in sediments. Comparative pathway analysis revealed the alteration of steroid hormone biosynthesis and retinol metabolism in B. aeruginosa after 90-day exposure to sediment-associated TBT at the concentration of 2000 ng/g dw, which might affect both reproduction and lipogenesis functions. The ubiquitin proteasome system and immune system might be the toxicity target in B. aeruginosa after exposure to sediment-associated TPT for 90 days.The results offered new mechanisms underlying the toxicity of sediment-associated tributyltin and triphenyltin.
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