Acute exposure to triphenyl phosphate (TPhP) disturbs ocular development and muscular organization in zebrafish larvae.

Triphenyl phosphate (TPhP) is an organophosphate flame retardant that is frequently detected in the environments. TPhP exposure is known to cause developmental toxicity. However, the underlying molecular mechanisms remain underestimated. In the present study, zebrafish embryos were acutely exposed to 0, 4 and 100 μg/L TPhP until 144 h post-fertilization. Profiles of differentially expressed proteins were constructed using a shotgun proteomic. With the input of differential proteins, principal component analysis suggested different protein expression profiles for 4 and 100 μg/L TPhP. Gene ontology and KEGG pathway analyses further found that effects of TPhP at 4 μg/L targeted phagosome and lysosome activity, while 100 μg/L TPhP mainly affected carbohydrate metabolism, muscular contraction and phagosome. Based on proteomic data, diverse bioassays were employed to ascertain the effects of TPhP on specific proteins and pathways. At gene and protein levels, expressions of critical visual proteins were significantly changed by TPhP exposure, including retinoschisin 1a, opsins and crystallins, implying the impairment of ocular development and function. TPhP exposure at 100 μg/L also altered the abundances of diverse muscular proteins and disordered the assembly of muscle fibers. Effects of TPhP on visual development and motor activity may be combined to disturb larval swimming behavior. In summary, current results provided mechanistic clues to the developmental toxicities of TPhP. Future works are inspired to broaden the toxicological knowledge of TPhP based on current proteomic results.