In recent decades, the decline in male reproductive capacity has become a global concern, with noticeable reductions in both semen quality and quantity. A growing body of research has linked increased levels of organic pollutants in the environment, such as traditional brominated flame retardants (BFRs), to reduced sperm quality. As BFRs are phased out, new alternatives like novel brominated flame retardants (NBFRs) are being widely used, but their health risks to ecosystems and human health remain poorly understood. 

Among these NBFRs, decabromodiphenyl ethane (DBDPE) stands out as the most widely produced and used in China. It has been frequently detected in the environment, wildlife, and human samples, raising concerns about its potential impact on male reproductive health. Exploring the response mechanisms of environmentally relevant concentrations of DBDPE on the male reproductive system is therefore critical.

Recently, a research group led by Prof. ZHOU Bingsheng from the Institute of Hydrobiology (IHB) of the Chinese Academy of Sciences has revealed thatDBDPE exposure could impair sperm quality and spermatogenesis, and the underlying mechanism could be attributed to DNA damage and energy metabolic reprogramming in testicular germ cells by shifting glycolysis to oxidative phosphorylation. This study was published in the Environmental Health Perspectives. 

In this research, zebrafish spermatozoa were treated with DBDPE (0.01, 0.1, 1, 10μM) for 3h, and the spermatozoa motility and fertilization ability with normal eggs were evaluated. The results showed that ex vivo exposure to DBDPE caused lower motility and fertilization rates of zebrafish spermatozoa. 

Subsequently, adult male zebrafish were treated with DBDPE (0.1, 1, 10, and 100 nM) for two months, and their reproductive performance was examined. It was found in vivo exposure to DBDPE caused lower sperm motility and abnormal spermatogenesis in male zebrafish testes. Integrated whole-proteome and phosphoproteome analysis revealed DNA damage responses and energy metabolic disorders in zebrafish testes, while lactate dehydrogenase (LDH), a key enzyme in energy metabolism, may be a potential target for DBDPE-induced reproductive dysfunction.

Finally, mouse spermatogonia GC-1 cells were exposed to DBDPE or oxamate (an LDH inhibitor) for 72 h, and their mechanisms of action were found to be similar. Seahorse assay further confirmed that DBDPE suppressed glycolysis by inhibiting LDH activity and enhanced oxidative phosphorylation, thereby reprogramming the energy metabolic process in germ cells. 

The study provides valuable insights into the reproductive toxicity of DBDPE and its potential mechanisms. It suggests that NBFRs such as DBDPE in the environment may represent a threat to the reproductive health of both aquatic organisms and human. 

The possible underlying mechanism of DBDPE-induced male reproductive disorder (Image by IHB)

(Editor: MA Yun)