Today’s trainee spotlight was written by Elana Elkin on the publication “Trichloroethylene metabolite S-(1,2-dichlorovinyl)-L-cysteine induces lipid peroxidation-associated apoptosis via the intrinsic and extrinsic apoptosis pathways in a first-trimester placental cell line.”
Authors: Elana R. Elkin, Sean M. Harris, Rita Loch-Caruso
Trichloroethylene (TCE) is a manmade chemical commonly used to clean grease off metal machine parts in industrial applications. Additionally, TCE is a chemical byproduct of commercial-level manufacturing of refrigerants used in car air conditioning systems. For decades, improper disposal of TCE allowed it to contaminate ground water and soil. This widespread contamination, coupled with its environmental persistence, has led to detection of TCE in a large number of Superfund sites. People can be exposed to TCE in a few different ways: inhalation of the vaporized chemical, ingestion through contaminated drinking water, or absorption through the skin. Once inside, the human body metabolizes TCE into several metabolites, and some of these metabolites exert harmful effect in the body. Several studies of pregnant women have demonstrated an association between maternal exposure to TCE and an increased risk of pregnancy complications such as babies born too soon or with low birth weight.
Our study investigated how exposure to the TCE metabolite S-(1, 2-dichlorovinyl)-L-cysteine (DCVC) may cause injury or death to a specific type of cell that plays a critical role in normal placental development. A healthy placenta is necessary for a normal pregnancy because it supplies the baby with oxygen and nutrients throughout the pregnancy until birth. Working with placental cells grown in the laboratory, our study showed that DCVC causes these cells to die prematurely through a specific form of cell death called apoptosis. Apoptosis is a tightly regulated intentional form of cell death that cells may undertake if they sense cellular damage or extremely stressful conditions such as exposure to a toxic chemical. In addition, we demonstrated that the antioxidant vitamin E can stop placental cells from undergoing DCVC-induced apoptosis. These findings show that these placental cells undergo premature apoptosis as a result of exposure to DCVC, suggesting that induction of apoptosis in the placenta may be one way in which exposure to TCE contributes to early abnormal placental development and adverse pregnancy outcomes. Our study provides new biological insights into the ways in which trichloroethylene exposure may contribute to abnormal placental development and resulting pregnancy complications, supporting prior reports in human populations. Further studies into the effects of this chemical on pregnancy are warranted.
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