Chromium VI − Induced developmental toxicity of placenta is mediated through spatiotemporal dysregulation of cell survival and apoptotic proteins

Environmental contamination with hexavalent chromium (CrVI) is a growing problem both in the U.S and developing countries. CrVI is a heavy-metal endocrine disruptor; women working in Cr industries exhibit an increased incidence of premature abortion and infertility. The current study was designed to...

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Published in:Reproductive toxicology (Elmsford, N.Y.) N.Y.), 2017-03, Vol.68, p.171-190
Main Authors: Banu, Sakhila K, Stanley, Jone A, Sivakumar, Kirthiram K, Arosh, Joe A, Taylor, Robert J, Burghardt, Robert C
Format: Article
Language:English
Subjects:
Animals
Apoptosis
Apoptosis - drug effects
Cell Survival - drug effects
Chromium - toxicity
Endocrine Disruptors - toxicity
Environmental Pollutants - toxicity
Female
Gestational Age
Hexavalent chromium
Maternal Exposure
Placenta
Placenta - drug effects
Placenta - metabolism
Placenta - pathology
Pregnancy
Rats, Sprague-Dawley
Spatio-Temporal Analysis
Trophoblasts
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Summary:Environmental contamination with hexavalent chromium (CrVI) is a growing problem both in the U.S and developing countries. CrVI is a heavy-metal endocrine disruptor; women working in Cr industries exhibit an increased incidence of premature abortion and infertility. The current study was designed to understand the mechanism of CrVI toxicity on placental cell survival/death pathways. Pregnant mothers were treated with or without CrVI (50ppmK2Cr2O7) through drinking water from gestational day (GD) 9.5–14.5, and placentas were analyzed on GD 18.5. Results indicated that CrVI increased apoptosis of trophoblasts, vascular endothelium of the metrial glands and yolk sac epithelium through caspase-3 and p53-dependent pathways. CrVI increased apoptosis in labyrinth and basal zones in a caspase-3-independent manner via AIF, and through an ATM-p53-NOXA-PUMA-p27 network. CrVI downregulated cell survival proteins Bcl-2, Bcl-XL and XIAP in the placenta. CrVI disrupts placental histoarchitecture and increases cell death by spatiotemporal modulation of apoptotic signaling.
ISSN:0890-6238
1873-1708
DOI:10.1016/j.reprotox.2016.07.006