Postnatal exposure to chromium through mother's milk accelerates follicular atresia in F1 offspring through increased oxidative stress and depletion of antioxidant enzymes.
Postnatal exposure to chromium through mother's milk accelerates follicular atresia in F1 offspring through increased oxidative stress and depletion of antioxidant enzymes.
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产后通过母乳接触铬会增加氧化应激和抗氧化酶的消耗，从而加速 F1 后代的卵泡闭锁。
DOI：
10.1016/j.freeradbiomed.2013.02.006
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发表时间：
2013
影响因子：
7.4
通讯作者：
Banu,SakhilaK
中科院分区：
文献类型：
--
作者：
Stanley,JoneA;Sivakumar,KirthiramK;Nithy,ThamizhK;Arosh,JoeA;Hoyer,PatriciaB;Burghardt,RobertC;Banu,SakhilaK
六价铬（CrVI）是一种重金属内分泌干扰物，被称为诱变剂、致畸剂和a类致癌物。CrVI污染的环境，包括饮用水，在美国30多个城市不断增加。CrVI在细胞内迅速转化为CrIII， CrIII可通过不同的机制导致DNA链断裂和癌症或细胞凋亡。我们之前的研究表明，哺乳期暴露于铬会导致F1雌性大鼠卵泡发育延迟或停止，类固醇激素水平下降，维生素c可以减轻（部分抑制）这两种情况。目前的研究验证了一个假设，即哺乳期暴露于CrIII会通过增加活性氧（ROS）和减少细胞抗氧化剂来加速F1后代的卵泡闭锁。结果显示，哺乳期暴露于CrIII剂量依赖性地增加了出生后25、45和65天的大鼠的卵泡闭锁和减少类固醇生成。维生素C在所有剂量下均可减轻或抑制中区填海第三期工程的影响。criiii增加血浆和卵巢过氧化氢和脂质过氧化氢；降低抗氧化酶（AOXs） GPx1、GR、SOD和过氧化氢酶；血浆和卵巢谷胱甘肽s转移酶升高。为了了解CrVI对卵巢颗粒（GC）和膜（TC）细胞室中ROS和AOXs的影响，我们在GC、TC和自发不朽颗粒细胞系（SIGC）中研究了细胞质和线粒体中SOD1、SOD2、过氧化氢酶、GLRX1、GSTM1、GSTM2、GSTA4、GR、TXN1、TXN2、TXNRD2和PRDX3等AOXs的ROS水平和mRNA表达。总体而言，CrVI下调了每个aox；维生素C能减轻CrVI对GCs和SIGCs中这些酶的影响，但不能减轻CrVI对TCs中GSTM1、GSTM2、TXN1和TXN2的影响。因此，这些数据首次揭示了哺乳期暴露于CrIII通过改变卵巢中ROS和AOXs的比例，加速了F1雌性后代的卵泡闭锁并减少了甾体生成。维生素C能够通过对GCs而不是TCs的保护作用来保护卵巢免受criiii诱导的氧化应激和卵泡闭锁。
Hexavalent chromium, CrVI, is a heavy metal endocrine disruptor, known as a mutagen, teratogen, and a group A carcinogen. Environmental contamination with CrVI, including drinking water, has been increasing in more than 30 cities in the United States. CrVI is rapidly converted to CrIII intracellularly, and CrIII can cause DNA strand breaks and cancer or apoptosis through different mechanisms. Our previous study demonstrated that lactational exposure to chromium results in a delay or arrest in follicle development and a decrease in steroid hormone levels in F1 female rats, both of which are mitigated (partial inhibition) by vitamin C. The current study tested the hypothesis that lactational exposure to CrIII accelerates follicle atresia in F1 offspring by increasing reactive oxygen species (ROS) and decreasing cellular antioxidants. Results showed that lactational exposure to CrIII dose-dependently increased follicular atresia and decreased steroidogenesis in postnatal day 25, 45, and 65 rats. Vitamin C mitigated or inhibited the effects of CrIII at all doses. CrIII increased hydrogen peroxide and lipid hydroperoxide in plasma and ovary; decreased the antioxidant enzymes (AOXs) GPx1, GR, SOD, and catalase; and increased glutathione S-transferase in plasma and ovary. To understand the effects of CrVI on ROS and AOXs in granulosa (GC) and theca (TC) cell compartments in the ovary, ROS levels and mRNA expression of cytosolic and mitochondrial AOXs, such as SOD1, SOD2, catalase, GLRX1, GSTM1, GSTM2, GSTA4, GR, TXN1, TXN2, TXNRD2, and PRDX3, were studied in GCs and TCs and in a spontaneously immortalized granulosa cell line (SIGC). Overall, CrVI downregulated each of the AOXs; and vitamin C mitigated the effects of CrVI on these enzymes in GCs and SIGCs, but failed to mitigate CrVI effects on GSTM1, GSTM2, TXN1, and TXN2 in TCs. Thus, these data for the first time reveal that lactational exposure to CrIII accelerated follicular atresia and decreased steroidogenesis in F1 female offspring by altering the ratio of ROS and AOXs in the ovary. Vitamin C is able to protect the ovary from CrIII-induced oxidative stress and follicle atresia through protective effects on GCs rather than TCs.
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影响因子：
4.1
作者：
Wise, Sandra S.;Holmes, Amie L.;Qin, Qin;Xie, Hong;Katsifis, Spiros P.;Thompson, W. Douglas;Wise, John Pierce, Sr.
通讯作者：
Wise, John Pierce, Sr.
对“通过口服途径定量评估六价铬的致癌性及其与人类暴露的相关性”的回应。
影响因子：
8.3
作者：
D. Proctor;C. Thompson;M. Suh;M. Harris
通讯作者：
M. Harris
影响因子：
--
作者：
J. Bonde
通讯作者：
J. Bonde
DOI：
--
发表时间：
1980
期刊：
Journal of Pharmacobio-Dynamics
影响因子：
--
作者：
Y. Sayato;K. Nakamuro;S. Matsui;M. Ando
通讯作者：
M. Ando
影响因子：
1.9
作者：
S. Ozdem;Cahit Nacitarhan;M. Gulay;F. Hatipoğlu;S. Ozdem
通讯作者：
S. Ozdem