The new brominated flame retardant decabromodiphenyl ethane (DBDPE) has been widely detected in a variety of environmental and biological media. Increasing evidence suggests that DBDPE may pose a risk of direct exposure to wildlife and human liver tissue. 

Previous studies on liver toxicity of DBDPE mainly focus on its effects on metabolic function, but the lack of the understanding of the effects and mechanisms of DBDPE on liver development and regeneration limits the evaluation of hepatotoxicity and the prediction of health risks.   

In a study published in Environmental Science & Technology, a research team led by Prof. ZHOU Bingsheng from the Institute of Hydrobiology (IHB) of the Chinese Academy of Sciences revealed the adverse effects and potential molecular mechanism of DBDPE on zebrafish liver development and regeneration.   

Using transgenic zebrafish Tg (fabp10a: dsRed; ela3l: EGFP) as a model, the researchers evaluated the effect of DBDPE on liver development and regeneration. The zebrafish embryos (two hours post fertilization, hpf) were exposed to DBDPE with different concentrations until 120 hpf.

They found that after DBDPE exposure, the fluorescence area and intensity of liver in larvae fish were significantly decreased, and the expression of hepatocyte marker gene fabp10a was decreased, indicating that DBDPE exposure would affect the early development of zebrafish liver. Further research showed that this may be related to cell cycle arrest and transcriptional suppression of genes related to liver development, such as gadd45ba.   

To characterize the effects on the regeneration process of the liver, PHx was performed on Tg (fabp10a: dsRed; ela3l: EGFP) zebrafish adults after 28 days exposure to DBDPE, and the liver recovery was observed under a fluorescence microscope at multiple time points (1, 7, 14, and 28 dps).

Liver regeneration curves showed that DBDPE exposure significantly inhibited the regeneration process of adult zebrafish liver. The adverse effects of DBDPE on liver regeneration were confirmed by the hepatosomatic ratio (HSI) of wild-type female adult fish and the immunofluorescence results of proliferating cell nuclear antigen.  

Through liver transcriptome analysis, the researchers found that abnormal cell proliferation regulation and lipid metabolism may be related to the inhibition of its regeneration process. This is the first study concerning the effects of DBDPE on liver regeneration.   

The findings of this study are helpful to the understanding of the hepatotoxicity of DBDPE and its potential mechanism, which in turn provides support for the ecological and health risk assessment of this and other emerging pollutants.