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芳烃受体及芳烃受体核转运蛋白信使核糖核酸与蛋白在大鼠和人类睾丸中的表达

Expression of aryl hydrocarbon receptor and aryl hydrocarbon receptor nuclear translocator messenger ribonucleic acids and proteins in rat and human testis.

作者信息

Schultz Rüdiger, Suominen Janne, Värre Tanja, Hakovirta Harri, Parvinen Martti, Toppari Jorma, Pelto-Huikko Markku

机构信息

Department of Developmental Biology, Tampere University, FIN-33014 Tampere, Finland.

出版信息

Endocrinology. 2003 Mar;144(3):767-76. doi: 10.1210/en.2002-220642.

Abstract

Dioxins, e.g. 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), use the aryl hydrocarbon receptor (AHR)/aryl hydrocarbon receptor nuclear translocator (ARNT) receptor complex to mediate their toxic actions. In addition to interaction with environmental pollutants, several transcription factors, steroid receptors, and growth factors are capable interacting with the AHR/ARNT complex, which suggests a constitutive role for the receptor complex. The testis has been reported to be among the most sensitive organs to TCDD exposure. Our experiments revealed a complex distribution of AHR and ARNT mRNAs and proteins in rat and human testis. AHR and ARNT immunoreactivities could be detected in the nuclei of interstitial and tubular cells. The incubation of seminiferous tubules in a serum-free culture medium resulted in up-regulation of AHR mRNA, which could be depressed by adding FSH to the culture medium. Furthermore, the incubation of tubular segments with a solution of 1 or 100 nM TCDD resulted in a 2- to 3-fold increase in apoptotic cells. Thus, up-regulation of AHR in cultured tubular segments and consecutive depression by FSH suggest a role for AHR in controlled cell death during spermatogenesis. We suggest that AHR and ARNT mediate effects by direct action on testicular cells in the rat and human testis.

摘要

二噁英,如2,3,7,8-四氯二苯并对二噁英(TCDD),利用芳烃受体(AHR)/芳烃受体核转运蛋白(ARNT)受体复合物来介导其毒性作用。除了与环境污染物相互作用外,几种转录因子、类固醇受体和生长因子也能够与AHR/ARNT复合物相互作用,这表明该受体复合物具有组成性作用。据报道,睾丸是对TCDD暴露最敏感的器官之一。我们的实验揭示了AHR和ARNT mRNA及蛋白在大鼠和人类睾丸中的复杂分布。在间质细胞和管状细胞的细胞核中可检测到AHR和ARNT免疫反应性。在无血清培养基中孵育生精小管会导致AHR mRNA上调,而向培养基中添加促卵泡激素(FSH)可抑制这种上调。此外,用1或100 nM TCDD溶液孵育管状节段会导致凋亡细胞增加2至3倍。因此,培养的管状节段中AHR的上调以及随后被FSH抑制表明AHR在精子发生过程中对细胞死亡的控制中起作用。我们认为AHR和ARNT通过直接作用于大鼠和人类睾丸中的睾丸细胞来介导效应。

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