2018
DOI: 10.1016/j.biochi.2018.03.002
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Lipidome-wide disturbances of human placental JEG-3 cells by the presence of MEHP

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Cited by 30 publications
(22 citation statements)
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“…These compounds have been demonstrated to cross the human placenta and reach the umbilical cord [ 81 ] and the amniotic fluid [ 82 ]. The altered placental development might be due to a peroxisome proliferator-activated receptor (PPAR)γ-mediated disruption in placental lipid metabolism, accounting for modified glycerolipids and glycerophospholipids levels, with a marked accumulation of triacylglycerols [ 83 ]. Furthermore, the presence of DEHP was also detected in maternal milk; thus, exposing newborns to these contaminants during breast feeding [ 84 ].…”
Section: Toxicological Aspects and Human Health Effectsmentioning
confidence: 99%
“…These compounds have been demonstrated to cross the human placenta and reach the umbilical cord [ 81 ] and the amniotic fluid [ 82 ]. The altered placental development might be due to a peroxisome proliferator-activated receptor (PPAR)γ-mediated disruption in placental lipid metabolism, accounting for modified glycerolipids and glycerophospholipids levels, with a marked accumulation of triacylglycerols [ 83 ]. Furthermore, the presence of DEHP was also detected in maternal milk; thus, exposing newborns to these contaminants during breast feeding [ 84 ].…”
Section: Toxicological Aspects and Human Health Effectsmentioning
confidence: 99%
“…Jukic et al revealed that pregnant females' exposure to excess di(2-ethylhexyl) phthalate (DEHP) was believed to increase the risk of developing early embryo loss [109]. MEHP changed the synthesis of lipidosomes in the JEG-3 human trophoblast cells leading to lipid imbalance [110]. Furthermore, Grindler et al investigated the methylation changes of 39 genes in first trimester placenta and found that most of the changes were negative [105].…”
Section: Phthalatesmentioning
confidence: 99%
“…In human cells, exposure to monoethylhexyl phthalate (MEHP) affected adipocyte size, possibly via increased lipolysis, glucose uptake, and oxygen consumption [31]. In placental cells MEHP produced lipidome-wide changes with specific alterations in glycerolipids and glycerophospholipids and promoted triacylglycerols accumulation [34]. Interestingly, prenatal DEHP exposure in rats was shown to target adrenal gland peroxisome proliferator-activated receptor (PPAR) and cholesterol biosynthesis pathways [33], which rendered offspring more susceptibility to second-hit stressor challenge [32].…”
Section: Discussionmentioning
confidence: 99%