Polychlorinated biphenyls impair endometrial receptivity in vitro via regulating mir-30d expression and epithelial mesenchymal transition.

Polychlorinated biphenyls (PCBs) are ubiquitous legacy persistent pollutants and epidemiological data showed that PCB burdens were associated with failed implantation in human. However, the mechanism how PCB exposure affects the embryo implantation is not clear. Using an in vitro model for human embryo implantation employing the human choriocarcinoma cell line JAR and the human endometrial cell line Ishikawa, we have shown that PCB mixture Aroclor 1254 at environmental-relevant concentrations (2.5, 12.5, and 62.5µM) dose-dependently impaired the endometrial receptivity by reducing the adhesion of JAR spheroid attachment and increasing the spheroid outgrowth. The receptive-up-regulated micro-RNA, mir-30d was also down-regulated in endometrial cells by the exposure. Following transient transfection of mir-30d mimic, the disrupted attachment and outgrowth of JAR spheroids was partially restored in the model. By measurement of cadherin switch and vimentin expression, the PCB exposure also activated epithelial mesenchymal transition (EMT) in endometrial cells. In accordance, mir-30d mimic suppressed the EMT markers induced by PCBs. Luciferase reporter assay confirmed that the EMT regulator Snai1 was targeted by mir-30d, and the expression of Snai1 was dose-dependently up-regulated by PCB exposure. Taken together, our study revealed that PCBs may affect the receptivity of endometrial cells by impairing the interaction between receptivity-up-regulated microRNA and EMT process.

Decrease in prosaposin in spermatozoon is associated with polychlorinated biphenyl exposure.

Polychlorinated biphenyls (PCBs) are a class of ubiquitous persistent organic pollutants and they have been associated with declining male fertility. In the present study, we aimed to determine the responsiveness of prosaposin (Psap) expression to PCB exposure. Male C57 mice were exposed to PCB mixture (Aroclor 1254) of environmental related doses by oral gavage. After exposure for 50 days, the expression of Psap was significantly decreased by PCB exposure in epididymides and epydidymal spermatozoa, but not in testis. The Psap abundance in sperm was decreased in a dose-dependent manner. Benchmark dose modeling revealed the 95% lower confidence limit on the benchmark dose (BMDL) and Benchmark Dose (BMD) for Psap reduction were 1.25 and 8.89 µg/kg Aroclor 1254, and for sperm motility reduction were 11.85 and 61.9 µg/kg Aroclor 1254. The depressed Psap level also showed a significant correlation (P<0.01, r=-0.531) with PCB accumulation in liver. In men with detectable PCB exposure in semen, Psap expression in sperm was significantly decreased whereas the semen parameters were unaffected. Linear regression showed that a negative association between total PCB level in seminal plasma and Psap level in ejaculated spermatozoa (P<0.05, r=-0.396). In conclusion, our data suggested that the abundance of Psap in sperm sample may be a sensitive endpoint to predict PCB exposure.

Antioxidant responses to benzo[a]pyrene, tributyltin and their mixture in the spleen of Sebasticus marmoratus.

It has been reported that there is an interaction between Benzo[a]pyrene (BaP), a widespread carcinogenic polycyclic aromatic hydrocarbon, and tributyltin (TBT), an organometal used as an antifouling biocide. This study was therefore designed to examine the potential in vivo influence of BaP, TBT and their mixture on splenic antioxidant defense systems of Sebastiscus marmoratus. The fish were exposed to water containing environmentally relevant concentrations of BaP, TBT and their mixture. Spleens were collected for biochemical analysis after exposure for 7, 25, 50 d and after recovery for 7, 20 d. Cotreatment with BaP and TBT for 7 d potentiated the induction of glutathione peroxidase (GPx) activity by BaP or TBT alone. The cotreatment for 25 and 50 d resulted in inhibition of GPx activity, which was similar to the effect of TBT. Splenic glutathione S-transferase (GST) activities were significantly elevated in S. marmoratus exposed to BaP starting from 7 d and remained high up to 25 d. However, no further activity change was found with prolonged exposure. Cotreatment of BaP and TBT primarily inhibited the GST activity, which was similar to the effect of TBT. Cotreatment with BaP and TBT for 25 or 50 d potentiated the depletion of GSH (glutathione) by BaP or TBT alone. MDA (malondialdehyde) contents in spleen of S. marmoratus were not significantly altered compared with the control during the test period. Spleen, as an immune organ, is sensitive to exposure of BaP or TBT. It should have an effective mechanism to counteract oxidative damage. Antioxidative defense systems in spleen of S. marmoratus should be considered as potential biomarkers. Short-term exposure of BaP or TBT could result in induction of antioxidant defense system. A significant decrease of these indices, such as GSH, GST, GPx might indicate more severe contamination.

[Epidemiological studies of sleep apnea-hypopnea syndrome: a questionnaire survey of Taiyuan].

OBJECTIVE: To obtain the epidemiological data of sleep apnea-hypopnea sydrome (SAHS) in Taiyuan. METHODS: A questionnaire survey was performed in 6 028 people living in Taiyuan. The prevalence of SAHS was estimated by a two-stage procedure. In the first stage, stratified cluster disproportional random sampling survey was performed in Taiyuan. 6 028 questionnaires were send to random sample of defined population in the 4 sites selected from 2 districts. The response rate was 85.11%. During the second stage 476 of those highly suspected of having SAHS (ESS >/= 9) underwent all-night polysomnographic (PSG) studies. RESULTS: From the study population, 179 were diagnosed as having SAHS. The overall prevalence was 3.5% (male 4.7% and female 1.9%). CONCLUSION: The prevalence of SAHS was 3.5% among Taiyuan.

Response of antioxidase in viscera of Pagrosuma major larvae to water soluble fraction of hydrocarbons in No.0 diesel oil.

Pagrosomus major larvae were exposed to the water-soluble fraction of hydrocarbon in No.0 diesel oil (corresponding to No.2 fuel oil) at concentrations of 0, 0.17, 1.22 and 8.82 mg/L for up to 15 days. Larvae were sampled on days 9 and 15 of the experiment. Supernatants of viscera tissue extractions were assayed for biochemical response in terms of oxidative stress-superoxide dismutase(SOD), activity of selenium-dependant glutathione peroxidase(Se-GPx) and catalase (Ca), and the concentration of reduced glutathione (GSH). On day 9 of exposure, statistically significant dose-related increases in Se-GPx and SOD activity, and GSH concentration were ohserved in all cases except for Se-GPx activity under the highest dosage of hydrocarbon. However, on day 15 of exposure, a similar dose-related response was only observed for Se-GPx activity. GSH concentration decreased and SOD activity showed no statistical difference as compared to controls. However, a significant decrease in compared to day 9 Se-GPx activity and GSH concentration, in contrast to increase SOD activity at day 15 as indicates an accelerated accumulation of H2O2 and potential oxidative damage under long-term exposure of larvae to hydrocarbons. No statistical changes were observed in Ca activity throughout the experiment, possibly owing to the high efficiency of Se-GPx. A recovery experiment was performed on indicating that the response of antioxidants measured tending to return to their control levels. These results prove the function of the antioxidant defense system of the larvae to the water-soluble fraction of hydrocarbons in No.0 diesel oil.