Inhibition of progesterone receptor activity in recombinant yeast by soot from fossil fuel combustion emissions and air particulate materials.
Numerous environmental pollutants have been detected for estrogenic activity by interacting with the estrogen receptor, but little information is available about their interactions with the progesterone receptor. In this study, emission samples generated by fossil fuel combustion (FFC) and air particulate material (APM) collected from an urban location near a traffic line in a big city of China were evaluated to interact with the human progesterone receptor (hPR) signaling pathway by examining their ability to interact with the activity of hPR expressed in yeast. The results showed that the soot of a petroleum-fired vehicle possessed the most potent anti-progesteronic activity, that of coal-fired stove and diesel fired agrimotor emissions took the second place, and soot samples of coal-fired heating work and electric power station had lesser progesterone inhibition activity. The anti-progesteronic activity of APM was between that of soot from petroleum-fired vehicle and soot from coal-fired establishments and diesel fired agrimotor. Since there was no other large pollution source near the APM sampling sites, the endocrine disrupters were most likely from vehicle emissions, tire attrition and house heating sources. The correlation analysis showed that a strong relationship existed between estrogenic activity and anti-progesteronic activity in emissions of fossil fuel combustion. The discoveries that some environmental pollutants with estrogenic activity can also inhibit hPR activity indicate that further studies are required to investigate potential mechanisms for the reported estrogenic activities of these pollutants.
Wang
Jingxian
J
Donghu Experimental Station of the Lake Ecosystems, The State Key Laboratory of Freshwater Ecology and Biotechnology, Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan. wangjx@ihb.ac.cn
Xie
Ping
P
Kettrup
Antonius
A
Schramm
Karl-Werner
KW
D000393:Air Pollutants; D002244:Carbon; D004391:Dust; D005579:Fossil Fuels; D015870:Gene Expression; D006801:Humans; D011374:Progesterone / Q000494:pharmacology; D011980:Receptors, Progesterone / Q000037:antagonists & inhibitors* / Q000235:genetics / Q000378:metabolism; D012441:Saccharomyces cerevisiae / Q000187:drug effects / Q000235:genetics / Q000378:metabolism; D014162:Transfection; D001335:Vehicle Emissions; D001616:beta-Galactosidase / Q000378:metabolism
D000393:Air Pollutants; D004391:Dust; D005579:Fossil Fuels; D011980:Receptors, Progesterone; D001335:Vehicle Emissions; D011374:Progesterone; D002244:Carbon; D001616:beta-Galactosidase