PMID: 

Int J Mol Sci. 2019 Dec 12 ;20(24). Epub 2019 Dec 12. PMID: 31842455

Abstract Title: 

The Mechanism of Bisphenol A Atherogenicity Involves Apolipoprotein A-I Downregulation through NF-κB Activation.

Abstract: 

Apolipoprotein A-I (apoA-I) is the major protein component of high-density lipoproteins (HDL), mediating many of its atheroprotective properties. Increasing data reveal the pro-atherogenic effects of bisphenol A (BPA), one of the most prevalent environmental chemicals. In this study, we investigated the mechanisms by which BPA exerts pro-atherogenic effects. For this, LDLRmice were fed with a high-fat diet and treated with 50µg BPA/kg body weight by gavage. After two months of treatment, the area of atherosclerotic lesions in the aorta, triglycerides and total cholesterol levels were significantly increased, while HDL-cholesterol was decreased in BPA-treated LDLRmice as compared to control mice. Real-Time PCR data showed that BPA treatment decreased hepatic apoA-I expression. BPA downregulated the activity of the apoA-I promoter in a dose-dependent manner. This inhibitory effect was mediated by MEKK1/NF-κB signaling pathways. Transfection experiments using apoA-I promoter deletion mutants, chromatin immunoprecipitation, and protein-DNA interaction assays demonstrated that treatment of hepatocytes with BPA induced NF-κB signaling and thus the recruitment of p65/50 proteins to the multiple NF-κB binding sites located in the apoA-I promoter. In conclusion, BPA exerts pro-atherogenic effects downregulating apoA-I by MEKK1 signaling and NF-κB activation in hepatocytes.

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PMID: 

Wei Sheng Yan Jiu. 2019 Nov ;48(6):964-975. PMID: 31875823

Abstract Title: 

[The role of GSK3β in adipose tissue inflammation induced by bisphenol-A in high fat diet fed mice].

Abstract: 

OBJECTIVE: To study the effect of glycogen synthase kinase 3β(GSK3β) in BPA-induced adipose tissue inflammation in high fat diet(HFD) fed mice.METHODS: Four-week-old male C57 BL/6 mice were randomly divided into normal diet(ND) group, HFD group, HFD + GSK3β inhibitor group, HFD + 1000 nmol/L BPA group, HFD+1000 nmol/L BPA+GSK3β inhibitor group. The mice were exposed to BPA via drinking water. From the 14 th week of BPA exposure to the end of 16 weeks, the GSK3β inhibitor group was intraperitoneally injected with 21. 5 mg/kg lithium chloride(Li Cl)every two days for a total of 10 times. At the end of 16 weeks, the mice were sacrificed after anesthesia, and the epididymal fat tissue was taken aseptically. The pathological changes were observed by H&E staining. The expressions of interleukin-1β(IL-1β) and tumor necrosis factor-α(TNF-α) were detected by immunohistochemistry(IHC). The expression of GSK3β protein and its S9 serine(GSK3β-S9) phosphorylation were detected by western blot.RESULTS: Compared with the ND group, the body weight [(34. 97±1. 91) g]and epididymal fat pad coefficient [(3. 25±0. 39) %]of HFD group was significantly up-regulated(P

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PMID: 

J Appl Toxicol. 2019 Dec 26. Epub 2019 Dec 26. PMID: 31875995

Abstract Title: 

The effects of different bisphenol derivatives on oxidative stress, DNA damage and DNA repair in RWPE-1 cells: A comparative study.

Abstract: 

Bisphenol A (BPA) is a well-known endocrine disruptor and it is widely used mainly in the plastics industry. Due to recent reports on its possible impact on health (particularly on the male reproductive system), bisphenol F (BPF) and bisphenol S (BPS) are now being used as alternatives. In this study, RWPE-1 cells were used as a model to compare cytotoxicity, oxidative stress-causing potential and genotoxicity of these chemicals. In addition, the effects of the bisphenol derivatives were assessed on DNA repair proteins. RWPE-1 cells were incubated with BPA, BPF, and BPS at concentrations of 0-600μM for 24 h. The inhibitory concentration 20 (IC, concentration that causes 20% of cell viability loss) values for BPA, BPF, and BPS were 45, 65, and 108μM, respectively. These results indicated that cytotoxicity potentials were ranked as BPA>BPF>BPS. We also found alterations in superoxide dismutase, glutathione peroxidase and glutathione reductase activities, and glutathione and total antioxidant capacity in all bisphenol-exposed groups. In the standard and modified Comet assay, BPS produced significantly higher levels of DNA damage vs the control. DNA repair proteins (OGG1, Ape-1, and MyH) involved in the base excision repair pathway, as well as p53 protein levels were down-regulated in all of the bisphenol-exposed groups. We found that the BPA alternatives were also cytotoxic and genotoxic, and changed the expressions of DNA repair enzymes. Therefore, further studies are needed to assess whether they can be used safely as alternatives to BPA or not.

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PMID: 

Immunopharmacol Immunotoxicol. 2019 Dec 26:1-9. Epub 2019 Dec 26. PMID: 31876196

Abstract Title: 

impact of bisphenol A on maturation and function of monocyte-derived dendritic cells in patients with primary Sjögren's syndrome.

Abstract: 

Epidemiological studies have shown that environmental factors accelerate the progress of primary Sjögren's syndrome (pSS). Bisphenol A (BPA), a classic endocrine disrupting chemical, affects the immune system. However, the impact of BPA on pSS has not yet been reported. The present study aimed to evaluate the potential relationship between BPA, estrogen receptor (ER), and pSS.We studied the impact of BPA on monocyte-derived dendritic cells (moDCs) from pSS patients and age-matched healthy controls (HCs). Morphological effects were observed under inverted microscope. Surface markers were analyzed by flow cytometry. ER and cytokine profiles were assessed using real-time polymerase chain reaction. The ability of moDCs to stimulate CD4T cells activation was assessed by mixed lymphocyte reaction (MLR).moDCs from both pSS patients and HCs expressed ERα as well as ERβ. After BPA-exposure, expression of ERα increased significantly in pSS patients, while that of ERβ remained unchanged. moDCs from BPA-exposed pSS patients showed irregular morphology and reduction in cell aggregation. BPA increased HLA-DR on moDCs of pSS patients via ERα, and promoted the secretion of IL6 and IL12. When co-cultured with BPA-treated moDCs, cytokines (IFN-γ, IL4, IL17, IL10) and transcription factors (T-bet, Gata3, RoR-γt, Foxp3) of CD4T cells showed imbalance of Th1/Th2/Th17/Treg polarization, with Th1 and Th17 dominating.BPA altered the function of moDCs through ERα, including antigen capture, secretion of inflammatory factors, and ability to stimulate T cells, as well as accelerated the progression and further deterioration of pSS.

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Low levels of testosterone can come with glaring symptoms such as erectile dysfunction and reduced bone mass. Before opting for hormone replacement therapy, learn about natural alternatives

PMID: 

Environ Sci Pollut Res Int. 2019 Dec 5. Epub 2019 Dec 5. PMID: 31732953

Abstract Title: 

Effects of di (2-ethylhexyl) phthalate and high-fat diet on lipid metabolism in rats by JAK2/STAT5.

Abstract: 

Exposure to di (2-ethylhexyl) phthalate (DEHP) induces lipid metabolism disorder and high-fat diet (HD) may have joint effects with DEHP. We aim to clarify the role of JAK2/STAT5 pathway in the process and reveal the effects of HD on the toxicity of DEHP. Wistar rats (160 animals) were fed with HD or normal diet (ND) respectively and exposed to DEHP 0, 5, 50, and 500 mg/kg/day for 8 weeks. Lipid levels, as well as the morphology of liver and adipose, mRNA levels, and protein levels of JAK2, STAT5A, STAT5B, FAS, ap2, and PDK4 were detected. The results showed that DEHP exposure leads to increased weight gain. The JAK2/STAT5 pathway was activated in adipose after DEHP exposure and promoted the expression of FAS, ap2, and PDK4 in ND rats. While in the liver, JAK2 was inhibited, and lipid synthesis and accumulation were increased. However, rats exposed to DEHP in combination with HD showed a complete disorder of lipid metabolism. Therefore, we conclude that DEHP affects lipid metabolism through regulating the JAK2/STAT5 pathway and promotes adipogenesis and lipid accumulation. High-fat diet may have a joint effect with DEHP on lipid metabolism disorder.

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PMID: 

Environ Sci Technol. 2019 Dec 17 ;53(24):14630-14637. Epub 2019 Dec 4. PMID: 31736299

Abstract Title: 

Exposure of Nail Salon Workers to Phthalates, Di(2-ethylhexyl) Terephthalate, and Organophosphate Esters: A Pilot Study.

Abstract: 

Relatively little is known about the exposure of nail technicians to semivolatile organic compounds (SVOCs) in nail salons. We collected preshift and postshift urine samples and silicone wrist bands (SWBs) worn on lapels and wrists from 10 female nail technicians in the Boston area in 2016-17. We analyzed samples for phthalates, phthalate alternatives, and organophosphate esters (OPEs) or their metabolites. Postshift urine concentrations were generally higher than preshift concentrations for SVOC metabolites; the greatest change was for a metabolite of the phthalate alternative di(2-ethylhexyl) terephthalate (DEHTP): mono(2-ethyl-5-carboxypentyl) terephthalate (MECPTP) more than tripled from 11.7 to 36.6μg/g creatinine. DEHTP biomarkers were higher in our study participants' postshift urine compared to 2015-2016 National Health and Nutrition Examination Survey females. Urinary MECPTP and another DEHTP metabolite were moderately correlated (= 0.37-0.60) with DEHTP on the SWBs, suggesting occupation as a source of exposure. Our results suggest that nail technicians are occupationally exposed to certain phthalates, phthalate alternatives, and OPEs, with metabolites of DEHTP showing the largest increase across a work day. The detection of several of these SVOCs on SWBs suggests that they can be used as a tool for examining potential occupational exposures to SVOCs among nail salon workers.

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PMID: 

Ecotoxicol Environ Saf. 2019 Nov 20:109944. Epub 2019 Nov 20. PMID: 31757513

Abstract Title: 

Association between phthalate exposure and blood pressure during pregnancy.

Abstract: 

BACKGROUND: Phthalates are endocrine disrupting chemicals (EDCs) that pose a serious hazard to the human health. Many epidemiological studies revealed a relationship between phthalates exposure and blood pressure in general population, while the relationship in pregnant women remains unknown.OBJECTIVES: Aimed to elucidate whether phthalate exposure is associated with blood pressure among pregnant women.METHODS: This study included 636 participants from Wuhan, China. Urine samples were conducted repeatedly in three trimesters, and 9 phthalates were measured in these samples. After each urine was sampled, all the participants completed blood pressure measurements. Associations between repeated measurements of phthalate concentration and blood pressure were evaluated by using generalized estimating equations. Stratified analysis by fetus gender was conducted.RESULTS: Among the pregnant women with male fetuses, mono-i-butyl phthalate (MiBP) exposed in the 1st trimester was associated with the increased diastolic blood pressure (DBP) measured in the 2nd trimester, while the environmental risk score (ERS) measured in the 1st and 2nd trimester was positively associated with systolic blood pressure (SBP) and DBP in the 2nd trimester. No significant relationships were observed among all the population or pregnant women with female fetuses.CONCLUSIONS: Exposure to higher levels of MiBP may be related to increased blood pressure during pregnancy in pregnant women with male fetuses.

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PMID: 

Front Pharmacol. 2019 ;10:1309. Epub 2019 Nov 6. PMID: 31780936

Abstract Title: 

Phthalate-Induced Fetal Leydig Cell Dysfunction Mediates Male Reproductive Tract Anomalies.

Abstract: 

Male fetal Leydig cells in the testis secrete androgen and insulin-like 3, determining the sexual differentiation. The abnormal development of fetal Leydig cells could lead to the reduction of androgen and insulin-like 3, thus causing the male reproductive tract anomalies in male neonates, including cryptorchidism and hypospadias. Environmental pollutants, such as phthalic acid esters (phthalates), can perturb the development and differentiated function of Leydig cells, thereby contributing to the reproductive toxicity in the male. Here, we review the epidemiological studies in humans and experimental investigations in rodents of various phthalates. Most of phthalates disturb the expression of various genes encoded for steroidogenesis-related proteins and insulin-like 3 in fetal Leydig cells and the dose-additive effects are exerted after exposure in a mixture.

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PMID: 

Int J Hyg Environ Health. 2019 Nov 26:113414. Epub 2019 Nov 26. PMID: 31784327

Abstract Title: 

Phthalate exposure increased the risk of early renal impairment in Taiwanese without type 2 diabetes mellitus.

Abstract: 

Studies have suggested that phthalates may be a risk factor for microalbuminuria, whereas little is known regarding their nephrotoxic effects on adults. We enrolled 311 participants (≥18 y, N = 241;

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