Activity

The total mass concentration of the measured analytes decreased by 93% during wastewater treatment. The analyte concentrations in the wastewater effluent were comparable to those measured in surface water 1 km downstream of the wastewater discharge point. Ultimately, the comprehensive method will serve as an important tool to inform the occurrence, fate, transport, and toxicity of a large suite of priority pharmaceuticals and pharmaceutical metabolites in natural and engineered systems. Cadmium (Cd) is widely present in the environment as a heavy metal poison. Prenatal Cd exposure can damage the placental glucocorticoid barrier, leading to foetal growth restriction (FGR), but the molecular mechanism is unknown. We aimed to study the effects of prenatal Cd exposure on 11β-HSD2 and its possible involvement in Cd induced damage in the placental glucocorticoid barrier. Pregnant rats were treated with CdCl2 (1.0 mg/kg/day) by gavage from gestational day (GD) 9-19. Maternal exposure to Cd increased the FGR rate of the offspring, and the levels of corticosterone in the placenta, maternal and foetal serum. Further in vitro experiments with placenta or JEG3 cells indicated that Cd was able to decrease 11β-HSD2 and Sp1 expression in trophoblast cells but did not affect 11β-HSD1. Additionally, decreased p300 and Sp1 enrichment at the 11β-HSD2 promoter region was observed in the cells treated with Cd. Decreasing or increasing Sp1 expression accordingly inhibited or promoted the expression of 11β-HSD2 and further decreased or increased p300 and Sp1 enrichment at the 11β-HSD2 promoter region. In conclusion, Cd inhibits the expression of 11β-HSD2 by affecting the binding of p300 to 11β-HSD2 via a decrease in Sp1 expression, which damages the placental glucocorticoid barrier and exposes the foetus to excessive glucocorticoids, resulting in FGR. These findings reveal a possible underlying molecular mechanism by which Cd exposure leads to FGR. Monitoring drinking water, including bottled water, is imperative to safeguarding public health especially where bottled water consumption is high like in the United Arab Emirates (UAE). In this study, radionuclide activity levels of Tritium (3H) and Potassium (40K) were assessed in various brands of bottled water marketed in UAE. Activity level data was used to calculate the annual effective doses (Ed) for different age groups, and the excess lifetime cancer risk (ELCR) for adult males and females in the UAE population. Activity levels for both radionuclides were below the allowable maximum guideline values specified by local and international standards. Calculated total age dependent ingestion doses revealed that adults and lactation age groups received the highest effective ingestion doses. Adult males exhibited a higher ELCR for both isotopes, compared to females. Nonetheless, total radioactive dose for each water brand (0.91-1.47 μSv/yr) as well as for each population group were well below the recommended annual reference dose level of 100 μSv set by World Health Organization. Therefore, bottled water in the UAE is safe from the radiological aspect for investigated radionuclides, and poses no significant radiological exposure and health risk to the public. KY 12420 datasheet The addition of different functional groups to ionic liquid anions or cations to synthesize task-specific ionic liquids (TSILs) according to specific needs has become a research hotspot. However, there are few studies on the toxicity of TSILs. We selected zebrafish (Danio rerio) to assess the toxicity of three TSILs 1-aminoethyl-3-methylimidazolium tetrafluoroborate ([C2NH2MIm]BF4), 1-methoxyethyl-3-methylimidazolium tetrafluoroborate ([MOEMIm]BF4) and 1-hydroxyethyl-3-methylimidazolium tetrafluoroborate ([HOEMIm]BF4). The 96 h median lethal concentration (96 h LC50) of the three TSILs [C2NH2MIm]BF4, [MOEMIm]BF4 and [HOEMIm]BF4 on zebrafish determined by an acute toxicity test were 143.8 mg/L, 2492.5 mg/L and 3086.7 mg/L, respectively. In the oxidative damage and DNA damage research experiments, zebrafish were exposed to [C2NH2MIm]BF4 (0, 5, 10, 20 and 40 mg/L), [MOEMIm]BF4 and [HOEMIm]BF4 (0, 1, 10, 50 and 100 mg/L) for 28 days, and levels of reactive oxygen species (ROS), superoxide dismutase (SOD), catalase (CAT), glutathione S-transferase (GST), malondialdehyde (MDA) and olive tail moment (OTM) in zebrafish liver were tested on days 7, 14, 21 and 28 after the exposure test. During the experiment, increased contents of ROS and MDA were detected; enzymatic activities especially SOD were inhibited; and DNA damage occurred in zebrafish. The toxicity of the three TSILs was compared by the integrated biomarker response (IBR). The toxicity order of three TSILs was [MOEMIm]BF4 > [HOEMIm]BF4 > [C2NH2MIm]BF4. In addition, this study can provide a toxicological basis for application research and the evaluation of functionalized ionic liquids with low toxicity in the future. The simultaneous adsorption and photocatalytic conversion of SO2 and NO on P25-TiO2 were studied. In particular, the interaction of SO2 and NO on each other’s adsorption and photocatalytic oxidation was discussed. The adsorption of NO on P25 was negligible when comparing to that of SO2, while with the coexistence of NO and SO2 in flue gas, both the adsorption of SO2 and NO were improved. In the presence of water and oxygen, the photocatalytic oxidation efficiency of NO with an efficiency of >69% was observed on irradiated TiO2 surface, which lasted for at least 1000 min. Oxygen was found to have much more important effect than water on the photocatalytic oxidation of NO. In the presence of SO2 however, the photocatalytic process of NO was largely reshaped. The whole process was controlled by the photocatalytic oxidation of SO2. A dramatic efficiency decease (breakthrough of the catalyst bed) was observed for both NO and SO2 due to the catalyst deactivation caused by the poisoning of SO2 oxidation products. Before the breakthrough, the photocatalytic conversion efficiency of NO increased with increasing the SO2 concentration, which was mainly due to the improved NO adsorption in the presence of SO2.