Growth inhibition of offspring larvae caused by the maternal transfer effects of tetrabromobisphenol A in zebrafish.

Tetrabromobisphenol A (TBBPA) is an industrial chemical and the most widely used brominated flame retardant, and has raised environmental health concerns. However, the maternal transfer toxicity of TBBPA is less studied in fish despite its frequency in the water environment, and limited evidence exists to confirm the major contributing factors. In this study, we performed a 28-d experiment on female and male zebrafish exposed to TBBPA (0, 5, 50, and 500 µg/L), and shortened body length of offspring larvae was observed at the maximum exposure concentration. By cross-mating control and exposed zebrafish (male or female), our results showed that the observed growth inhibition in the progeny was attributed to the maternal transfer effect. Although 28-d exposure resulted in the existence of TBBPA in ovaries and ova, the maternal transfer of TBBPA was not responsible for the shortened body length of offspring larvae, as evidenced through TBBPA embryo microinjection. Moreover, proteomic analyses in ova indicated that the abundance of apolipoproteins (apoa1, apoa1b, apoa2, apoa4b, and apoc1) was significantly downregulated in the ova, which may be partially responsible for the shortened body length of offspring larvae. Interestingly, these proteins did not differentially express in the ovaries. Therefore, our results demonstrate that TBBPA exposure disturbed maternal protein transfer from the ovaries to the ova, providing novel insights into the underlying maternal transfer effects.

Exposure of adult zebrafish (Danio rerio) to Tetrabromobisphenol A causes neurotoxicity in larval offspring, an adverse transgenerational effect.

Tetrabromobisphenol A (TBBPA) is one of the most extensively used brominated flame retardants and is universally detected in the environment. However, information related to its transgenerational toxicity is sparse. Using zebrafish as a study model, adult fish were exposed to TBBPA at different concentrations (0, 3, 30, or 300 µg/L) for 42 d and then, the exposed adults were spawned in TBBPA-free water. The neurobehavior of adults and larval offspring was evaluated, and the levels of thyroxine (T4), triiodothyronine (T3) and neurotransmitters (acetylcholine, dopamine and gamma-aminobutyric acid) were quantified in larvae and embryos. Our results showed that TBBPA was detected in embryo and the locomotor activity of larval offspring was significantly reduced, suggesting that TBBPA can transfer to offspring and result in neurotoxicity in larval offspring. Furthermore, a reduction in T3 levels was observed in both the larvae and embryos. We also found a significantly decreased content of dopamine in larval offspring, accompanied by downregulated mRNA expression of rdr2b and drd3. Our results demonstrated that TBBPA can be transferred to offspring embryos, and subsequently induce neurotoxicity in larval offspring by affecting the amount of T3 transferred from the parents to embryos and the production of dopamine in larvae.