In recent decades, the decline in male reproductive capacity has become a global concern. 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, alternatives like novel brominated flame retardants (NBFRs) are being widely used. 

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.

In a study published in Environmental Health Perspectives, a research group led by Prof. ZHOU Bingsheng from the Institute of Hydrobiology (IHB) of the Chinese Academy of Sciences 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. 

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

Then, researchers examined the reproductive performance of adult male zebrafish which were treated with DBDPE (0.1, 1, 10, and 100 nM) for two months. The results showed that in vivo exposure to DBDPE caused lower sperm motility and abnormal spermatogenesis. 

Integrated whole-proteome and phosphoproteome analysis revealed DNA damage responses and energy metabolic disorders, while lactate dehydrogenase (LDH), a key enzyme in energy metabolism, may be a potential target for DBDPE-induced reproductive dysfunction.

In mouse models, researchers found that the exposure of mouse spermatogonia GC-1 cells to DBDPE or oxamate (an LDH inhibitor) for 72 h had similar mechanisms of action. 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 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.