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首页> 外文会议>International symposium on halogenated persistent organic pollutants >STUDIES ON THE MOLECULAR MECHANISMS OF 2,3,7,8-TETRACHLORODIBENZO-p-DIOXIN–INDUCED MORPHOLOGICAL ABNORMALITIES IN THE DEVELOPING MOUSE KIDNEY
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STUDIES ON THE MOLECULAR MECHANISMS OF 2,3,7,8-TETRACHLORODIBENZO-p-DIOXIN–INDUCED MORPHOLOGICAL ABNORMALITIES IN THE DEVELOPING MOUSE KIDNEY

机译：2,3,7,8-四氯二苯并偶氮对二恶英在发育中的小鼠肾脏中引起的形态学异常的分子机理研究

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摘要

The developing rodent kidney is one of the most sensitive tissues to the toxic effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). The aim of the present study was to evaluate the etiology of hydronephrosis by focusing on the mechanisms of TCDD-induced morphological abnormalities in mouse pup kidneys through measuring gene expression of several factors involved in nephrogenesis. Mouse neonates were exposed to TCDD through milk of dams that had received 15 μg TCDD/kg body weight orally after delivery. In this time-course study, the critical period of susceptibility for development of hydronephrosis was postnatal days (PND) 1–4. In the vehicle-treated mice, mRNAs for insulin-like growth factor (IGF)II, and transforming growth factor (TGF)-β were expressed at maximum levels for the first 2 days after birth and gradually decreased with advancing development. TCDD was found to cause up-regulation of TGF-β expression and down-regulation of IGFII in the early postnatal period. Furthermore, TCDD significantly up-regulated the cyclin-dependent kinase inhibitors p27kip1 and p57kip2 in developing kidneys. Studies using AhR-null mice showed that the up-regulation of p57kip2 mRNA was AhR dependent. Taken together, these data suggest that the hydronephrotic lesion caused by TCDD could be mediated by TCDD-induced G1 cell cycle arrest through mechanisms involving the AhR.
机译：发育中的啮齿动物肾脏是对2,3,7,8-四氯二苯并-p-二恶英（TCDD）毒性作用最敏感的组织之一。本研究的目的是通过重点研究TCDD诱导的小鼠幼仔肾脏形态异常的机制来评估肾积水的病因，方法是测量参与肾发生的几种因素的基因表达。小鼠新生儿通过分娩后口服接受15μgTCDD / kg体重的母乳暴露于TCDD。在此时程研究中，肾积水易感性的关键时期是产后天数（PND）1-4。在用载体治疗的小鼠中，胰岛素样生长因子（IGF）II和转化生长因子（TGF）-β的mRNA在出生后的前两天以最高水平表达，并随着发育的发展而逐渐降低。发现TCDD在出生后早期引起TGF-β表达的上调和IGFII的下调。此外，TCDD显着上调了发育中肾脏中细胞周期蛋白依赖性激酶抑制剂p27kip1和p57kip2的表达。使用AhR空小鼠的研究表明p57kip2 mRNA的上调是AhR依赖性的。综上所述，这些数据表明由TCDD引起的肾积水病变可以通过涉及AhR的机制由TCDD诱导的G1细胞周期停滞来介导。

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  • 会议地点 Beijing(CN)
  • 作者

    Nishimura N; Miyata C; Qing W; Fujimaki H; Nishimura H;

  • 作者单位

    Research Center for Environmental Risk,National Institute for Environmental Studies,Tsukuba,305-8506 Japan;

    Research Center for Environmental Risk,National Institute for Environmental Studies,Tsukuba,305-8506 Japan College of Environmental Health,Azabu University,Sagamihara,229-8501 Japan;

    School of Public Health,Fudan University,Shanghai,200032 China;

    Research Center for Environmental Risk,National Institute for Environmental Studies,Tsukuba,305-8506 Japan;

    Human Sciences,Aichi Mizuho University,Toyota,470-0394 Japan;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 环境分析化学;
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