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持续接触六价铬会损害Wistar大鼠后代的青春期发育和卵巢组织结构。

Persistent hexavalent chromium exposure impaired the pubertal development and ovarian histoarchitecture in wistar rat offspring.

作者信息

Samuel Jawahar B, Stanley Jone A, Sekar Pasupathi, Princess Rajendran A, Sebastian Maria S, Aruldhas Michael M

机构信息

Department of Zoology, St. John's College, Thirunelveli, TN 627002, India.

出版信息

Environ Toxicol. 2014 May;29(7):814-28. doi: 10.1002/tox.21810. Epub 2012 Aug 31.

Abstract

Hexavalent chromium (CrVI) is a highly toxic metal and a major environmental pollutant. Several studies indicate that CrVI exposure adversely affects reproductive function. We reported that maternal Cr exposure resulted in Cr accumulation in the reproductive organs of female offsprings. CrVI can cross the placental barrier and also can be passed through breastfeeding. The present investigation aimed to determine the persistent (in utero through puberal period) CrVI exposure-induced toxic effects on the reproductive functions of mother and the offspring. Induction of oxidative stress is one of the plausible mechanisms behind Cr-induced cellular deteriorations. Mother rats exposed to CrVI showed reduced reproductive outcome, while the offsprings showed higher accumulation of Cr in ovary, altered steroid, and peptide hormones. Specific activities of antioxidant enzymes were decreased and associated with increased levels of H2 O2 , and lipid peroxidation. CrVI exposure also damaged the ovarian histoarchitecture in various age groups studied. CrVI exposure also delayed the sexual maturation. Results from the present investigation suggest that CrVI exposure from in utero through puberal period significantly damaged the pubertal development through altered antioxidants, anemia, and altered hormone levels. These changes were associated with damaged ovarian histoarchitecture and extended estrous cycle in developing Wistar rats.

摘要

六价铬(CrVI)是一种剧毒金属,也是主要的环境污染物。多项研究表明,接触CrVI会对生殖功能产生不利影响。我们曾报道,母体接触铬会导致雌性后代生殖器官中铬的积累。CrVI可穿过胎盘屏障,也可通过母乳喂养传递。本研究旨在确定从子宫内到青春期持续接触CrVI对母体和后代生殖功能的毒性作用。氧化应激的诱导是铬诱导细胞退化背后的一种可能机制。接触CrVI的母鼠生殖结果降低,而后代卵巢中铬的积累增加,类固醇和肽类激素发生改变。抗氧化酶的比活性降低,并与过氧化氢和脂质过氧化水平的升高有关。在研究的各个年龄组中,CrVI暴露还破坏了卵巢组织结构。CrVI暴露还延迟了性成熟。本研究结果表明,从子宫内到青春期接触CrVI会通过改变抗氧化剂、贫血和激素水平,显著损害青春期发育。这些变化与发育中的Wistar大鼠卵巢组织结构受损和发情周期延长有关。

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