Prenatal exposure to chromium induces early reproductive senescence by increasing germ cell apoptosis and advancing germ cell cyst breakdown in the F1 offspring.
Prenatal exposure to chromium induces early reproductive senescence by increasing germ cell apoptosis and advancing germ cell cyst breakdown in the F1 offspring.
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DOI：
10.1016/j.ydbio.2014.02.003
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发表时间：
2014-04-01
影响因子：
2.7
通讯作者：
Banu, Sakhila K.
中科院分区：
文献类型：
--
作者：
Sivakumar, Kirthiram K.;Stanley, Jone A.;Arosh, Joe A.;Pepling, Melissa E.;Burghardt, Robert C.;Banu, Sakhila K.
六价铬（CrVI）是毒性较强的重金属之一，广泛应用于Chrome电镀、焊接、木材加工、制革等50多个行业。作为世界领先的铬化合物生产国之一，美国在保护人类健康免受CrVI多种不利影响方面面临着越来越大的挑战。CrVI在细胞内迅速转化为CrIII，并可通过不同的机制诱导细胞凋亡。我们以前的研究表明，出生后暴露于CrVI导致卵泡发育和青春期延迟或停滞。妊娠大鼠从妊娠第9.5天至第14.5天通过饮用水接受25 ppm重铬酸钾（CrVI）处理，在GD 20时取出胎盘，估计胎盘中的总Cr;在出生后第-1天（PND）从F1后代中取出卵巢，并进行各种分析。我们的结果表明，妊娠期暴露于CrVI导致（i）胎盘中的Cr浓度增加，（ii）通过上调p53/p27-Bax-caspase-3蛋白和增加p53-SOD-2共定位来增加生殖细胞凋亡;（iii）加速生殖细胞囊肿（GCC）分解;（iv）促进原始卵泡组装和初级卵泡转变，以及（v）下调p-AKT、p-ERK和XIAP。作为上述事件的结果，CrVI诱导早期生殖衰老和减少产仔数的F1雌性后代。
Hexavalent chromium (CrVI), one of the more toxic heavy metals, is widely used in more than 50 industries such as chrome plating, welding, wood processing and tanneries. As one of the world’s leading producers of chromium compounds, the U.S. is facing growing challenges in protecting human health against multiple adverse effects of CrVI. CrVI is rapidly converted to CrIII intracellularly, and can induce apoptosis through different mechanisms. Our previous studies demonstrated postnatal exposure to CrVI results in a delay or arrest in follicle development and puberty. Pregnant rats were treated with 25 ppm potassium dichromate (CrVI) from gestational day (GD) 9.5 to 14.5 through drinking water, placentae were removed on GD 20, and total Cr was estimated in the placentae; ovaries were removed from the F1 offspring on postnatal day (PND)-1 and various analyses were performed. Our results show that gestational exposure to CrVI resulted in (i) increased Cr concentration in the placenta, (ii) increased germ cell apoptosis by up-regulating p53/p27–Bax–caspase-3 proteins and by increasing p53–SOD-2 co-localization; (iii) accelerated germ cell cyst (GCC) breakdown; (iv) advanced primordial follicle assembly and primary follicle transition and (v) down regulation of p-AKT, p-ERK and XIAP. As a result of the above events, CrVI induced early reproductive senescence and decrease in litter size in F1 female progeny.
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影响因子：
4
作者：
Cecconi, Sandra;Rossi, Gianna;Macchiarelli, Guido
通讯作者：
Macchiarelli, Guido
影响因子：
4
作者：
El Mouatassim, S;Guérin, P;Ménézo, Y
通讯作者：
Ménézo, Y
影响因子：
12.4
作者：
De Felici, M;Di Carlo, A;Piacentini, M
通讯作者：
Piacentini, M
影响因子：
13.3
作者：
De Felici, Massimo;Lobascio, Anna Maria;Klinger, Francesca Gioia
通讯作者：
Klinger, Francesca Gioia
影响因子：
3.8
作者：
Collins, Bradley J.;Stout, Matthew D.;Hooth, Michelle J.
通讯作者：
Hooth, Michelle J.