• Vance Creech posted an update 6 months ago

    Among these, we propose the previously recognized metabolite norsertraline, sertraline ketone and hydroxy-sertraline. All the remaining biotransformation products are herein reported for the first time. The removal efficiency of approximately 94% was determined after the treatment in the flow-through bioreactors. To support our findings, we sampled influents and effluents from two wastewater treatment plants and untreated wastewater from a psychiatric hospital. Removal efficiencies of 81% and 77% were determined, and along with the parent compound sertraline, the presence of eight transformation products was confirmed in the actual wastewaters.Background Copper is an essential microelement for animals and has been used at pharmacological doses in weaned piglets to improve growth performance. However, it also induces systemic oxidative stress after short-term feeding. The aim of this study was to investigate the effects of dose and duration of dietary copper on lipid peroxidation and oxidative stress status in model of weaned piglets. Methods A total of 48 crossbred piglets (weaned at 21d, weight ∼8.2 kg) were randomly assigned into 4 groups of 12 in each. The control group and 3 treatment groups fed with basal diet supplemented with 20, 100 and 200 mg/kg copper as copper sulfate for 3 and 6 weeks, respectively. Results Dietary copper supplementation significantly affected the activities of ALP, LDH, LIPC and the levels of Ca and TG in serum as well as the copper and zinc deposition in liver. Increased MDA concentrations, and decreased GPX, CP and CAT concentrations in serum were found in 0, 100 and 200 mg Cu/kg diet groups at 3 weeks post weaning. Hepatic lipid peroxidation was also induced in these groups indicated from hepatic SOD1, GPX1, CAT, CP, MT1A and MT2A transcriptional levels. Those adverse symptoms were alleviative at 6 weeks post weaning. The hepatic Cu and Zn concentrations, serum MDA concentrations, and serum CAT and GPX activities were significantly correlated with Actinobacillus, Lactobacillus, Sarcina, Helicobacter, Campylobacterales, which could affect the intestinal health further. Conclusion These results indicated that copper deficiency or over supplementation would affect the systemic lipid peroxidation. These adverse changes were not observed when the dietary copper concentration at 20 mg Cu/kg diet. The results suggested the appropriate dietary copper concentration is around 20 mg Cu/kg diet, and its range might be much stricter than we thought.Objective To explore the relationships between serum copper levels and overweight/total obesity and central obesity in children and adolescents. Methods We included 2,000 children and adolescents from the 2011-2016 US National Health and Nutrition Examination Surveys. The multivariable linear model, logistic model and restricted cubic splines were adopted to assess the relationships. Models were adjusted for data release cycle, age, sex, race/ethnicity, ratio of family income to poverty, and dietary intakes of protein, total sugars, total fat, fiber, energy, calcium, vitamin D, vitamin C, and hours watch television or videos. Results The prevalences of overweight/total obesity and central obesity were 37.38% and 33.40%, respectively. For per-quintile increment in serum copper levels, body mass index increased by 1.06 (0.79-1.33) (kg/m2) and waist circumference increased by 2.43 (1.58-3.27) (cm). The odds ratios (95% confidence intervals) for overweight/total obesity and central obesity among participants with the highest quintile compared with those with the lowest quintile of serum copper levels were 5.46 (3.31-8.98) and 5.64 (3.31-9.58), respectively. The above-mentioned associations were not modified by age (children 6-12 years, adolescents 13-18 years) and sex. Dose-response analysis showed that the odds of overweight/total obesity and central obesity increased with increasing serum copper levels to a level of approximate 140 ug/dL where the association seemed to reach a plateau, respectively. Conclusions Serum copper levels were positively associated with body mass index and waist circumference, and elevated serum copper levels were associated with higher odds of overweight/total obesity and central obesity in children and adolescents.Aims The increase in the usage of copper nanoparticles (Cu NPs) in the industrial and medical fields has raised concerns about their possible adverse effects. The present study aims to investigate the potential adverse effects of Cu NPs on the brain of adult male Wistar rats through the estimation of some oxidative stress parameters and acetylcholinesterase (AChE) activity. Basic procedures Cu NPs were prepared and characterized using different techniques Dynamic Light Scattering, X-Ray Diffraction, Transmission and Scanning Electron Microscopy, Fourier transform Infrared Spectroscopy, in addition to Energy Dispersive X-ray Spectroscopy. Rats were divided into two groups Cu NPs-treated group (IV injected with 15 mg/kg ˷ 13 nm Cu NPs for 2 successive days) and a control group (injected with saline). Rats of the 2 groups were decapitated simultaneously after 48 h of the last injection. The Cu content in different brain areas was analyzed using inductively coupled plasma mass spectrometry. Moreover, the effect of Cu NPs on brain edema was evaluated. The behavior of rats in an open-field was also examined 24 h post the last injection. Main findings Significant increases of Cu content in the cortex, cerebellum, striatum, thalamus and hippocampus were found. Moreover, Cu NPs lead to the induction of oxidative stress condition in the thalamus, hypothamaus and medulla. In addition, Cu NPs induced significant increases in AChE activity in the medulla, hippocampus, striatum besides midbrain. Cu NPs-injected rats showed also decreased exploratory behaviour. Principal conclusion The results obtained in the present study point to the importance of toxicity assessments in evaluating the efficiency of Cu NPs for the safe implementation in different applications.Background Over-exposure to manganese (Mn) causes irreversible movement disorders with signs and symptoms similar, but not identical, to idiopathic Parkinson’s disease (IPD). Recent data suggest that Mn toxicity occurs in dopaminergic (DA) neurons, although the mechanism remains elusive. This study was designed to investigate whether Mn interfered the apoptotic signaling transduction cascade in DA neurons. DDO-2728 cell line Methods Mouse midbrain dopaminergic MN9D cells were exposed to Mn in a concentration range of 0, 400, 800, or 1200 μM as designated as control, low, medium, and high exposure groups, respectively. The flow cytometry with Annexin V/PI double staining and immunohistochemistry were used to assess the apoptosis. Results Data indicated that Mn exposure caused morphological alterations typical of apoptosis, increased apoptotic cells by 2-8 fold, and produced reactive oxidative species (ROS) by 1.5-2.2 fold as compared to controls (p less then 0.05). Studies by qPCR and Western blot revealed that Mn exposure significantly increased the protein expression of extracellular signal-regulated kinase-5 (ERK5) and mitogen-activated ERK kinase-5 (MEK5) (p less then 0.

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