Assessment of source water contamination by estrogenic disrupting compounds in China

Detection of estrogenic disrupting compounds（EDCs） in drinking waters around China has led to rising concerns about health risks associated with these compounds.There is,however,a paucity of studies on the occurrence and identification of the main compounds responsible for this pollution in the source waters.To fill this void,we screened estrogenic activities of 23 source water samples from six main river systems in China,using a recombinant two-hybrid yeast assay.All sample extracts induced significant estrogenic activity,with E2 equivalents（EEQ） of raw water ranging from 0.08 to 2.40 ng/L.Additionally,16 samples were selected for chemical analysis by gas chromatography-mass spectrometry.The EDCs of most concern,including estrone（E1）,17β-estradiol（E2）,17α-ethinylestradiol（EE2）,estriol（E3）,diethylstilbestrol（DES）,estradiol valerate（EV）,4-t-octylphenol（4-t-OP）,4-nonylphenols（4-NP） and bisphenol A（BPA）,were determined at concentrations of up to 2.98,1.07,2.67,4.37,2.52,1.96,89.52,280.19 and 710.65 ng/L,respectively.Causality analysis,involving comparison of EEQ values from yeast assay and chemical analysis identified E2,EE2 and 4-NP as the main responsible compounds,accounting for the whole estrogenic activities（39.74% to 96.68%）.The proposed approach using both chemical analysis and yeast assay could be used for the identification and evaluation of EDCs in source waters of China.

A gas chromatography/mass spectrometry method for the simultaneous analysis of 50 phenols in wastewater using deconvolution technology

Phenolic compounds exist widely in the influents and effluents of sewage treatment plants (STPs) and most are un-regulated.In this study,a gas chromatography-mass spectrometry (GC-MS) method for the simultaneous analysis of 50 phenolic compounds in wastewater was developed.Deconvolution technology was used to identify contaminants that are covered by co-extracted materials.A mass spectral library containing all 50 silylated phenolic compounds was first established and used for deconvolution.Twelve typical phenolic compounds were selected to optimize the sample preparation procedures.Solid-phase extraction using a C18 cartridge coupled with an HLB cartridge was used for pre-concentration and dichloromethane was used for elution.The solutes were derivatized and analyzed by GC-MS.The blank and matrix spike recoveries ranged from 57.46% to 136.4% and 47.87% to 114.8%,respectively.Method detection limits ranged from 3.64 to 97.64 ng L–1.The relative standard deviations of all the recovery experiments were lower than 13.6%.The instrument limits of quantification ranged from 0.7 to 87.7 pg.The method has been applied to analyze the influents and effluents of 5 Chinese STPs.Except for regulated phenolic compounds (phenol and 2,4,6-trichlorophenol),three un-regulated phenolic compounds,including 2-chlorophenol,2,5-dichlorophenol and 2,4-dichloro3-ethyl-6-nitrophenol were identified in the effluent wastewater.The detected concentrations of un-regulated phenolic compounds could possibly cause environmental effects,indicating that immediate attention is required to prevent complications.

In vitro assay for human thyroid hormone receptor β agonist and antagonist effects of individual polychlorinated naphthalenes and Halowax mixtures

Polychlorinated naphthalenes (PCNs) are dioxin-like environmental contaminants. There is growing concern over the endocrine-disrupting effects of PCNs, but very few studies have investigated the effect of PCNs on the thyroid system. This study used a yeast two-hybrid assay, which included the recombinant human thyroid receptor(TR)-β and reporter genes, to characterize the TRβ-disrupting effects of five individual PCN congeners, five PCN Halowax mixtures, and naphthalene. Their agonist and antagonist effects were studied in the absence and presence of 5×10-7 mol/L 3,3′,5-triiodo-L-thyronine, which induced submaximal β-galactosidase activity. Naphthalene, 1,2,3,4,5,6,7,8-octachloronaphthalene and all of the Halowax mixtures (Halowax 1000, 1001, 1013, 1014 and 1099) showed no agonist or antagonist activity on TRβ at the concentrations tested (up to 10-2 g/L). The lighter PCN congeners, namely 1-chloronaphthalene, 2-chloronaphthalene, 1,4-dichloronaphthalene and 1,2,3,4-tetrachloronaphthalene showed no agonist activity but showed significant antagonist activity on TRβ. The 20% relative inhibitory concentrations of these PCNs were less than 9.13 × 10-3 g/L. Thus, bioaccumulation of these lighter PCN congeners may disrupt the thyroid hormone system and inhibit TR-mediated cellular responses. Studies in the future should investigate the possible associations between the presence PCNs and adverse health outcomes.

Cellular and molecular mechanisms in vascular repair after traumatic brain injury:a narrative review

Traumatic brain injury(TBI)disrupts normal brain function and is associated with high morbidity and fatality rates.TBI is characterized as mild,moderate or severe depending on its severity.The damage may be transient and limited to the dura matter,with only subtle changes in cerebral parenchyma,or life-threatening with obvious focal contusions,hematomas and edema.Blood vessels are often injured in TBI.Even in mild TBI,dysfunctional cerebral vascular repair may result in prolonged symptoms and poor outcomes.Various distinct types of cells participate in vascular repair after TBI.A better understanding of the cellular response and function in vascular repair can facilitate the development of new therapeutic strategies.In this review,we analyzed the mechanism of cerebrovascular impairment and the repercussions following various forms of TBI.We then discussed the role of distinct cell types in the repair of meningeal and parenchyma vasculature following TBI,including endothelial cells,endothelial progenitor cells,pericytes,glial cells(astrocytes and microglia),neurons,myeloid cells(macrophages and monocytes)and meningeal lymphatic endothelial cells.Finally,possible treatment techniques targeting these unique cell types for vascular repair after TBI are discussed.