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Trichloroacetate‐Induced Developmental Toxicity and the Production of Reactive Oxygen Species in Zebrafish Embryos ( Danio rerio )
Author(s) -
Issa Omar N,
Hassoun Ezdihar A,
Williams Frederick E
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.lb648
Subject(s) - zebrafish , danio , developmental toxicity , hatching , embryo , toxicity , human fertilization , andrology , reactive oxygen species , biology , chemistry , anatomy , biochemistry , microbiology and biotechnology , zoology , medicine , genetics , fetus , pregnancy , organic chemistry , gene
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 (LD 50 ) 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 .