No abstract

To assess the developmental toxicity of trichloroacetate (TCA), zebrafish embryos were exposed to 8 to 48 mM of TCA and evaluated for developmental milestones from 8‐ to 144‐hour postfertilization (hpf). All developmental toxicities are reported in this paper. Embryos were found to have developed edema in response to 16 to 48 mM of TCA exposure at 32‐ to 80‐hpf, experienced delay in hatching success in response to 24 to 48 mM at 80‐hpf. Lordosis was observed in developing embryos exposed to 40 to 48 mM at 55‐ to 144‐hpf. The observed toxic effects of TCA exposure were found to be concentration and exposure period independent. Effects were found to be associated with increases in superoxide anion production, but these increases were also found to be concentration and time independent. TCA resulted in concentration‐dependent increases in embryonic lethality at 144‐hpf, with an LC50 determined to be 29.7 mM.

Trichloroacetic acid (TCA) is one of the toxic haloacetate by‐products formed as a result of the chlorination of drinking water as a part of the disinfection process. In this report, the developmental toxic effects of TCA were investigated in a nonmammalian vertebrate species: zebrafish (Danio rerio) embryos. The exposure of zebrafish embryos to (24, 32, 40, and 48 mM) TCA occurred at 4 hours post‐fertilization (hpf), and the embryos were monitored at 8, 24, 32, 55, 80, and 144 hpf for developmental landmarks from proper gastrulation to swimming and feeding success. At 32 hpf, TCA elicited a significant YSE at all of TCA concentrations when compared with the untreated controls. However, when compared with the untreated controls at the 55 and 80 hpf, a significant amount of CSE and YSE was observed in animals exposed to all of the tested TCA concentrations. Hatching delay was also produced in zebrafish embryos due to exposure to TCA concentrations of 24 and 40 mM at the 55hpf developmental time point. The hatching delay was more pronounced at the 55 hpf than 80 hpf time point. In addition, embryos developed lordosis resulting in behavioral abnormalities like abnormal feeding and swimming. The lethal dose‐50 (LD50) of TCA in zebrafish embryos was calculated as 29.72 mM. Along with the induced developmental toxicity, TCA elicited the release of superoxide anion (SA) in zebrafish embryos at 32, 55, and 80 hpf of development.The reactive oxygen species (ROS) produced by TCA exposure coincides with the developmental abnormalities which were observed in exposed embryos. This indicates that the ROS generated may cause the developmental toxic effects of TCA exposure in zebrafish embryos.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.