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    Please use this identifier to cite or link to this item: http://tkuir.lib.tku.edu.tw:8080/dspace/handle/987654321/53532

    Title: Nephrotoxicity assessments of acetaminophen during zebrafish embryogenesis
    Authors: Peng, Hsi-Chu;Wang, Yun-Hsin;Wen, Chi-Chung;Wang, Wei-Hua;Cheng, Chien-Chung;Chen,Yau-Hung
    Contributors: 淡江大學數學學系;淡江大學化學學系
    Keywords: Acetaminophen;Fluorescent;Kidney;Nephrotoxicity;Transgenic;Zebrafish;共變量測量誤差;柯斯模型;半母數最大概似估計;剖面概似函數
    Date: 2010-05
    Issue Date: 2011-05-20 09:42:19 (UTC+8)
    Publisher: Philadelphia: Elsevier Inc.
    Abstract: We used a green fluorescent kidney line, Tg(wt1b:GFP), as a model to access the acetaminophen (AAP)-induced nephrotoxicity dynamically. Zebrafish (Danio rerio) embryos at different developmental stages (12–60 hpf) were treated with different dosages of AAP (0–45 mM) for different time courses (12–60 h). Results showed that zebrafish embryos exhibited no evident differences in survival rates and morphological changes between the mock-treated control (0 mM) and 2.25 mM AAP-exposure (12–72 hpf) groups. In contrast, after higher doses (22.5 and 45 mM) of exposure, embryos displayed malformed kidney phenotypes, such as curved, cystic pronephric tube, pronephric duct, and a cystic and atrophic glomerulus. The percentages of embryos with malformed kidney phenotypes increased as the exposure dosages of AAP increased. Interestingly, under the same exposure time course (12 h) and dose (22.5 mM), embryos displayed higher percentages of severe defects at earlier developmental stage of exposure (12–24 hpf), whereas embryos displayed higher percentages of mild defects at later exposure (60–72 hpf). With an exposure time course less than 24 h of 45 mM AAP, no embryo survived by the developmental stage of 72 hpf. These results indicated that AAP-induced nephrotoxicity depended on the exposure dose, time course and developmental stages. Immunohistochemical experiments showed that the cells' morphologies of the pronephric tube, pronephric duct and glomerulus were disrupted by AAP, and consequently caused cell death. Real-time RT-PCR revealed embryos after AAP treatment decreased the expression of cox2 and bcl2, but increased p53 expression. In conclusion, AAP-induced defects on glomerulus, pronephric tube and pronephric duct could be easily and dynamically observed in vivo during kidney development in this present model.
    Relation: Comparative Biochemistry and Physiology Part C: Toxicology & Pharmacology 151(4), pp.480-486
    DOI: 10.1016/j.cbpc.2010.02.004
    Appears in Collections:[Graduate Institute & Department of Mathematics] Journal Article
    [Graduate Institute & Department of Chemistry] Journal Article

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