Insights into the mechanisms of tris(2-chloroethyl) phosphate-induced growth inhibition in juvenile yellow catfish Pelteobagrus fulvidraco.

Abstract

With the gradual elimination of brominated flame retardants (BFRs), the production and application of tris (2-chloroethyl) phosphate (TCEP), as a substitute of BFRs, has increased greatly. The objective of the present study was to comprehensively explore the potential adverse effects of TCEP on fish growth and the possible underlying mechanisms. To this end, juvenile yellow catfish (Pelteobagrus fulvidraco) were exposed to environmentally relevant concentrations of TCEP (0, 1, 10 and 100 µg/L) for 30 days. The results showed that exposure to high concentrations of TCEP (10 and 100 µg/L) significantly decreased body weight, body length and specific growth rate (SGR). Plasma IGF-I levels and hepatic mRNA levels of igf1 and igf1r were all reduced, while the transcriptional levels of IGFBPs (igfbp2, igfbp3, igfbp5) were significantly up-regulated in the liver of yellow catfish under exposure to 10 and 100 µg/L TCEP. TCEP-induced growth inhibition might be related to somatostatin (SS) signaling system, as evidenced by elevated mRNA transcriptions of ss in brain and its receptors (sstr2, sstr3, sstr5) in liver. In addition, fish exposed to high concentrations of TCEP displayed multiple histological alterations in liver. Taken together, these findings suggested that TCEP (>10 µg/L) might exert its inhibitory effect on fish growth through interfering with the GH/IGF axis and SS signaling system, and by impairing hepatic structures.