Levels of phthalate acid esters and sex hormones and their possible sources in traffic-patrol policemen in Chongqing

Lu, Lu; Rong, Honghui; Wang, Chong; Cui, Bo; Huang, Yujing; Tan, Yao; Zhang, Ling; Peng, Yi; García, José Manuel Pérez; Chen, Jian

doi:10.1007/s11356-019-04265-4

Cited by 9 publications

(1 citation statement)

References 34 publications

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“…A wide range of concentrations was selected according to DEP and its main metabolite (monoethyl phthalate—MEP) quantification in human biological samples [ 4 , 20 , 21 , 22 , 23 ], previous phthalates studies [ 24 , 25 , 26 , 27 , 28 ], and the in vitro–in vivo scaling factor [ 29 ]. This is defined as the need to have in vitro concentrations 20- to 200-fold higher than the maximum concentration observed in the human plasma in order to cause similar biological effects.…”

Section: Methodsmentioning

confidence: 99%

Exposure to DEP Modifies the Human Umbilical Artery Vascular Resistance Contributing to Hypertension in Pregnancy

Mariana,

Soares,

Castelo-Branco

et al. 2024

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Hypertensive disorders in pregnancy (HDP) are the most prevalent diseases during pregnancy. In addition to the already identified risk factors, exposure to environmental contaminants has been also considered a new one. Phthalates, which are classified as priority environmental pollutants due to their ubiquitousness and endocrine disrupting properties, have been implicated in HDP in some epidemiological studies. Nevertheless, phthalates’ vascular impacts still need to be clarified. Thus, we aimed to understand the connection between phthalates exposure and the occurrence of gestational hypertension, as well as the pathway involved in the pathological vascular effects. We investigated diethyl phthalate’s (DEP) effect on the vascular reactivity of the human umbilical arteries (HUAs) from normotensive and hypertensive pregnant women. Both DEP’s nongenomic (within minutes effect) and genomic (24 h exposure to DEP) actions were evaluated, as well as the contribution of cyclic guanosine monophosphate and Ca2+ channel pathways. The results show that short-term exposure to DEP interferes with serotonin and histamine receptors, while after prolonged exposure, DEP seems to share the same vasorelaxant mechanism as estrogens, through the NO/sGC/cGMP/PKG signaling pathway, and to interfere with the L-type Ca2+ channels. Thus, the vascular effect induced by DEP is similar to that observed in HUA from hypertensive pregnancies, demonstrating that the development of HDP may be a consequence of DEP exposure.

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