Exposure to tributyltin and triphenyltin induces DNA damage and alters nucleotide excision repair gene transcription in Sebastiscus marmoratus liver

Tributyltin (TBT) and triphenyltin (TPT) coexist in the aquatic environment. However, the effects of TBT, TPT and a mixture of the two on DNA damage in marine fish livers and the mechanism involved remain to be elucidated. In the present study, we assessed their ability to cause hepatic DNA damage in Sebastiscus marmoratus liver and we investigated the related mechanism. The results showed that TBT, TPT and the mixture significantly decreased liver DNA integrity in a dose-dependent manner. Using Pearson correlation coefficient analysis, we identified that the hepatic total tin concentration was significantly correlated with hepatic DNA integrity after exposure to TBT alone and combined exposure to TBT and TPT. In order to clarify the mechanism which influences DNA repair, the mRNA levels of nucleotide excision repair (NER) genes were determined using real-time PCR analysis. The results showed that NER gene expression levels were disturbed. The expression of XPB, ERCC1, and DNA Pol ɛ was significantly decreased after treatment with TBT, TPT and the mixture, while the expression of PCNA, HR23B, XPG, and DNA lig III was significantly increased in treated-groups compared to the control. Based on this, we proposed that TBT, TPT and a mixture of the two induced DNA damage in marine fish livers by altering the transcription levels of the NER genes.

► Tributyltin (TBT) and triphenyltin (TPT) coexist in the aquatic environment.
► TBT, TPT and a mixture of the two at environmentally relevant concentrations caused hepatic DNA damage in a dose-dependent manner.
► The induced DNA damage in marine fish livers caused by the TBT, TPT and a mixture of the two was due to altering the transcription levels of the NER genes.