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睾丸DAAM1表达在锌对镉诱导的雄性大鼠生殖毒性的保护作用中的参与。

Involvement of testicular DAAM1 expression in zinc protection against cadmium-induced male rat reproductive toxicity.

作者信息

Chemek Marouane, Venditti Massimo, Boughamoura Sana, Mimouna Safa B, Messaoudi Imed, Minucci Sergio

机构信息

LR11ES41: Génétique, Biodiversité et Valorisation des Bioressources, Institut de Biotechnologie, Université de Monastir, Monastir, Tunisia.

Dipartimento di Medicina Sperimentale, Sez. Fisiologia Umana e Funzioni Biologiche Integrate "F. Bottazzi", Università della Campania Luigi Vanvitelli, Napoli, Italy.

出版信息

J Cell Physiol. 2018 Jan;233(1):630-640. doi: 10.1002/jcp.25923. Epub 2017 May 19.

Abstract

In order to verify the effects of exposure to Cd and Zn on testicular DAAM1 gene and protein expression and also to ascertain their involvement in the protective role of Zn in prevent the testicular toxicity Cd-induced in male offspring rats at adult age after gestational and lactational exposure, male offspring rats, from mothers receiving either tap water, Cd, Zn, or Cd + Zn during gestation and lactation periods, were scarified on postnatal days (PND) 70. The reproductive organ (testis, epididymis, and vesicle seminal) were collected, weighed, and analyzed. The results showed that exposure to Cd in utero and through lactation decreased the relative reproductive organ weight, altered the testicular histology at the interstitial and tubular levels, and causing a significant reduction in the daily sperm production (DSP) per testis and per gram of testis, and other then altering the epididymal sperm quality. Furthermore, both mRNA and protein expression of rat testicular DAAM1 were also inhibited in Cd-treated group. Zn supply has completely corrected the most of these toxic effects. Our results imply that Zn could prevent Cd-induced testicular toxicity and sperm quality alteration in adult male rat after gestational and lactational exposure, probably via the restoration of the testicular DAAM1 expression inhibited by Cd.

摘要

为了验证镉(Cd)和锌(Zn)暴露对睾丸DAAM1基因和蛋白表达的影响,并确定它们在锌对孕期和哺乳期暴露的成年雄性后代大鼠镉诱导的睾丸毒性的保护作用中的参与情况,在出生后第70天处死了来自在孕期和哺乳期接受自来水、镉、锌或镉+锌处理的母亲的雄性后代大鼠。收集、称重并分析生殖器官(睾丸、附睾和精囊)。结果表明,子宫内和哺乳期暴露于镉会降低生殖器官相对重量,改变睾丸间质和小管水平的组织学结构,导致每个睾丸和每克睾丸的每日精子产量(DSP)显著降低,并改变附睾精子质量。此外,镉处理组大鼠睾丸DAAM1的mRNA和蛋白表达也受到抑制。锌的供应完全纠正了这些毒性作用中的大部分。我们的结果表明,锌可能通过恢复被镉抑制的睾丸DAAM1表达,预防孕期和哺乳期暴露的成年雄性大鼠镉诱导的睾丸毒性和精子质量改变。

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