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Environmental Pollutant Polybrominated Diphenyl Ether, a Flame Retardant, Induces Primary Amnion Cell Senescence
Faranak Behnia1, Morgan R Peltier2, George R Saade1
1Division of Maternal-Fetal Medicine and Perinatal Research, Department of Obstetrics and Gynecology, University of Texas Medical Branch at Galveston, Galveston, TX, USA.
Insights
Polybrominated diphenyl ethers (PBDEs) cause oxidative stress, leading to cell senescence and inflammation, increasing preterm birth (PTB) risk. PBDE-99 showed a more pronounced effect than PBDE-47 in human amnion cells.
Area of Science:
- Environmental Health
- Reproductive Biology
- Toxicology
Background:
- Polybrominated diphenyl ethers (PBDEs) are flame retardants linked to spontaneous preterm birth (PTB).
- The mechanism may involve oxidative stress (OS), fetal cell senescence, and inflammation.
Purpose of the Study:
- To investigate the effects of PBDEs on human amnion epithelial cells.
- To determine if PBDEs induce oxidative stress, senescence, and inflammation.
Main Methods:
- Primary amnion epithelial cells were exposed to PBDE congeners 47 and 99.
- Assessed reactive oxygen species (ROS) kinetics, cell morphology, p38 MAPK activation, senescence (SA β-gal), and COX-2 expression.
Main Results:
- Both PBDEs rapidly induced ROS.
- PBDE-99 significantly activated p38 MAPK and increased COX-2 expression.
- PBDEs induced cell death-associated morphology and senescence, with PBDE-99 having a stronger effect.
Conclusions:
- PBDEs induce congener-dependent oxidative stress, p38 MAPK activation, senescence, and inflammation in human amnion cells.
- These findings support PBDEs as environmental pollutants contributing to PTB pathways.
Objective:
Polybrominated diphenyl ethers (PBDEs) are documented to increase the risk for spontaneous preterm birth (PTB). We hypothesize that PBDEs cause oxidative stress (OS) that leads to fetal cell senescence and inflammation associated with PTB.
Methods:
Primary amnion epithelial cells (n = 5) isolated from term, not in labor pregnancies, were exposed to PBDE congeners 47 and 99 (each 5 μM). ROS kinetics was monitored. Morphologic changes, phospho-p38 MAPK (P-p38) activation, development of senescence, and induction of uterotonins (COX-2 expression) were quantified using light microscopy, Western blot, senescence-associated β-galactosidase (SA β-gal) staining, and qRT-PCR, respectively, after 48 and 72 hr of exposure.
Results:
Both PBDE congeners induced ROS within 2 min compared to controls (P < 0.05). P-p38 activation was significant after PBDE-99 treatment than controls (P < 0.05). After 72 hr of treatment, both PBDE-treated cells showed cell death-associated morphologic changes with significantly higher SA β-gal-stained cells than control. COX-2 expression was higher after 72 hr of treatment with PBDE-99. Overall, the PBDE-99 response was more pronounced than PBDE-47.
Conclusions:
Congener-dependent OS response, p38 MAPK activation, senescence, and COX-2 expression were seen in human amnion cells by PBDEs. These findings demonstrate environment pollutant-induced senescence activation and inflammation can lead to pathways resulting in PTB.
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