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Fluoride is a widespread environmental pollutant that at high levels exerts numerous deleterious effects on human health. The toxic effects of fluoride are a matter of serious concern since many countries have regions of endemic fluorosis. The main source of fluoride exposure for humans is intake of contaminated groundwater. Fluoride is absorbed from the gastrointestinal tract and enters the circulating blood, where the abundant red blood cells (RBC) are an early and major target of fluoride toxicity. Chronic fluoride exposure generates free radicals, reactive species which leads to redox imbalance, cytotoxicity and hematological damage. This study aimed to determine the effect of sodium fluoride (NaF) on human RBC under in vitro conditions. Isolated RBC were incubated with different concentrations of NaF (10-500 µM) for 8 h at 37 °C. Several biochemical parameters were determined in hemolysates or whole cells. Treatment of RBC with NaF enhanced the generation of reactive oxygen and nitrogen species. This increased the oxidation of hemoglobin to yield methemoglobin and oxoferrylhemoglobin, which are inactive in oxygen transport. NaF treatment increased the degradation of heme causing release of free iron from its porphyrin ring. NHWD-870 order Cellular antioxidant power was significantly decreased in NaF-treated RBC, lowering the metal reducing and free radical quenching ability of cells. The two pathways of glucose metabolism in RBC i.e. glycolysis and hexose monophosphate shunt, were inhibited. NaF also inhibited the plasma membrane redox system, and its associated ascorbate free radical reductase, to disrupt transmembrane electron transport. These results suggest that fluoride generates reactive species that cause extensive oxidative modifications in human RBC.Hepatic oxidative stress, as one important mechanism of cadmium (Cd)-induced hepatic toxicity, could, as known, be ameliorated by vitamin E (VE). However, the underlying mechanism remains to be elucidated. To investigate whether the antioxidant vitamin E can protect against Cd-induced sub-chronic liver injury associated with oxidative stress and nuclear factor erythrocyte 2-related factor 2 (Nrf2) pathway, male Sprague-Dawley rats (nine-week-old) were randomly divided into four groups (eight rats/group), namely, control, VE (100 mg/kg VE), Cd (5 mg/kg CdCl2) and VE+Cd (100 mg/kg VE+5 mg/kg CdCl2), and received intragastric administration of Cd and/or VE for four weeks. Cd-exposure alone resulted in reduced liver weight, liver histological alteration and oxidative stress, accumulation of Cd in the liver, elevated ALT and AST concentrations in serum together with decreased mRNA and protein expressions of Nrf2 pathway related molecules (Nrf2, HO-1, NQO-1, GCLC, GCLM and GST). However, the co-treatment of Cd and VE significantly ameliorated the changes mentioned above, and promoted the expression of genes and proteins of Nrf2 pathway related molecules in comparison to the Cd-exposure alone. Our results indicate that the protective effect of VE against Cd-induced sub-chronic hepatic damage in rats is associated with the inhibition of oxidative stress and activation of Nrf2 pathway.With the wide application of neodymium oxide nanoparticles (NPs-Nd2O3) in various fields, their health hazards have aroused public concern in recent years. However, data regarding the cytotoxicity of NPs-Nd2O3 is limited. In this study, we investigated the function and mechanism of long-chain non-coding RNAs (lncRNAs) in NPs-Nd2O3-induced airway inflammation. Treatment with NPs-Nd2O3 induced an inflammatory response in human bronchial epithelial cells (16HBE) by upregulating the expression of interleukin-6 (IL-6) and interleukin-8 (IL-8). The levels of LDH and intracellular ROS in the cells treated by various doses of NPs-Nd2O3 also increased significantly. After treatment with 10 μg/ml NPs-Nd2O3, RNA microarray and real-time quantitative polymerase chain reaction (qRT-PCR) showed a significant upregulation of lncRNA loc105377478. Functional experiments suggested lncRNA loc105377478 enhanced the expression of IL-6, IL-8 and ROS in NPs-Nd2O3-treated 16HBE cells, and it was further demonstrated that lncRNA loc105377478 promoted the activation of NF-κB by negatively regulating ADIPOR1 expression. Moreover, the expression of IL-6 and IL-8 in NPs-Nd2O3-treated 16HBE cells was regulated by lncRNA loc105377478, which was mediated by the NF-κB signaling pathway. In conclusion, lncRNA loc105377478 promotes NF-κB activation by negatively regulating ADIPOR1 expression, thereby upregulating the expression of IL-6 and IL-8 in 16HBE cells treated with NPs-Nd2O3.Lead (Pb) is one of the most toxic heavy metal environmental pollutants due to its widespread use of the industry and it is a harmful substance for human and animal health. This study was conducted to investigate the potential protective effects of ellagic acid (EA) on performance, egg quality, antioxidant parameters, and apoptotic pathway proteins in laying quails exposed to Pb toxicity. A total of 168 (15-week old) laying quails (Coturnix coturnix Japonica) were divided into 6 experimental groups (with similar initial average body weight). Birds were fed 1 of 6 diets for 8 weeks 1 - Control (basal diet), 2 - Pb (basal diet + 100 mg/kg Pb), 3 - EA-300 (basal diet + 300 mg/kg EA), 4 - EA-500 (basal diet + 500 mg/kg EA), 5 - Pb + EA-300 (basal diet + 100 mg/kg Pb + 300 mg/kg EA), 6 - Pb + EA-500 (basal diet + 100 mg/kg Pb + 500 mg/kg EA). The results showed that adding 100 mg/kg of Pb to basal diet was adversely affected the performance parameters and, feed intake and egg production were significantly decreased by Pb supplementation (P 0.05). Liver and kidney tissues of Pb group malondialdehyde (MDA) level increased (P less then 0.001) and, GSH, GSH-Px, and CAT values decreased (P less then 0.001) but, EA supplementation alleviated this condition (P less then 0.001). The protein levels of caspase-3 and -9 were significantly increased in the Pb group compared to the control group, whereas EA supplementation alleviated the Pb-induced apoptosis by decreasing caspase-3 and -9 levels in the liver tissue (p less then 0.001). In laying quails exposed to Pb toxicity, EA supplementation improves the performance parameters, enhances the antioxidant defense system, and suppresses apoptosis via regulates the expression of caspase-3 and -9. Thus, it was concluded that EA (especially 500 mg/kg) can ameliorate the toxic effects of Pb exposure in quails.The present study aimed to explore the effect of synthetic and naturally occurring chelators, EDTA and citric acid (CA), respectively, on changes in physiological and biochemical factors including cell death, level of mercury ions accumulation, malondialdehyde (MDA) content, total phenol and total flavonoids, anthocyanins and DPPH free radical scavenging activity, in the leaves of okra (Abelmoschus esculentus L.) plants exposed to mercury stress. In addition, polyphenolic compounds profile was assessed by high-performance liquid chromatography. The okras were planted in completely controlled hydroponic conditions (Hoagland solution). After they reached the four-leaf stage, they were treated simultaneously with different concentrations of HgCl2, EDTA and CA chelators, and their combination for one month. At the stage of maturity, the physiological and biochemical factors of the plant leaves were measured. The results showed that with the application of higher concentration of HgCl2, cell death, level of shoot d with mercury. In addition, EDTA and CA can play a significant role in removing this toxic metal through transferring it from the culture medium to the plant.Mancozeb is a metal-containing ethylene bis-dithiocarbamate fungicide widely used in agriculture. Ethylene thiourea (ETU) is the primary metabolite of Mancozeb. Mancozeb has been associated with spontaneous abortions and abnormal menstruation in women. However, the effects of Mancozeb and ETU on embryo attachment remain unknown. The human blastocyst surrogate trophoblastic spheroids (JEG-3), endometrial epithelial surrogate adenocarcinoma cells (Ishikawa), or human primary endometrial epithelial cells (EECs) monolayer were used in the spheroid attachment models. Ishikawa and EECs were pretreated with different concentrations of Mancozeb or ETU for 48 h before the attachment assay. Gene expression profiles of Ishikawa cells were examined to understand how Mancozeb modulates endometrial receptivity with Microarray. The genes altered by Mancozeb were confirmed by qPCR and compared with the ETU treated groups. Mancozeb and ETU treatment inhibited cell viability at 10 μg/mL and 5000 µg/mL, respectively. At non-cytotoxic concentrations, Mancozeb at 3 μg/mL and ETU at 300 μg/mL reduced JEG-3 spheroid attachment onto Ishikawa cells. A similar result was observed with human primary endometrial epithelial cells. Mancozeb at 3 μg/mL modified the transcription of 158 genes by at least 1.5-fold in Microarray analysis. The expression of 10 differentially expressed genes were confirmed by qPCR. Furthermore, Mancozeb decreased spheroid attachment possibly through downregulating the expression of endometrial estrogen receptor β and integrin β3, but not mucin 1. These results were confirmed in both overexpression and knockdown experiments and co-culture assay. Mancozeb but not its metabolite ETU reduced spheroid attachment through modulating gene expression profile and decreasing estrogen receptor β and integrin β3 expression of endometrial epithelial cells.This is a novel study about responses of leaf photosynthetic traits and plant mercury (Hg) accumulation of rice grown in Hg polluted soils to elevated CO2 (ECO2). The aim of this study was to provide basic information on the acclimation capacity of photosynthesis and Hg accumulation in rice grown in Hg polluted soil under ECO2 at day, night, and full day. For this purpose, we analyzed leaf photosynthetic traits of rice at flowering and grain filling. In addition, chlorophyll content, soluble sugar and Malondialdehyde (MDA) of rice leaves were measured at flowering. Seed yield, ear number, grain number per ear, 1000-grain weight, total mercury (THg) and methylmercury (MeHg) contents were determined after harvest. Our results showed that Hg polluted soil and ECO2 had no significant effect on leaf chlorophyll content and leaf mass per area (LMA) in rice. The contents of soluble sugar and MDA in leaves increased significantly under ECO2. Mercury polluted soil treatment significantly reduced the light saturated CO2 assimilation rate (Asat) of rice leaves only at flowering, but not at grain filling. Night ECO2 greatly improved rice leaf water use efficiency (WUE). ECO2 greatly increased seed yield and ear number. In addition, ECO2 did not affect THg accumulation in rice organs, but ECO2 and Hg treatment had a significant interaction on MeHg in seeds, husks and roots.In this work level of Polycyclic Aromatic Hydrocarbon (PAHs) from indoor Environment Tobacco Smoke (ETS) of pubic bars in Nigeria was investigated. Indoor air samples were obtained from different public bars using Polyurethane foam (PUF) passive samplers. Analysis of PAHs was carried out using GC-MS operated in selected ion monitoring mode. Result showed the average concentration range of 2.71-9.69 ng/m3 while the ∑ 16 PAHs range from 43.43 to 155.11 ng/m3. The incremental lifetime cancer risk (ILCR) values from inhalation of PAHs in these bars ranged from 2.4×10-7-5.2×10-7 while non-carcinogenic risk, Hazard Quotient (HQ) ranged from 2×10-4-4.5×10-4. Although these values are lower than WHO permissible limit, nevertheless the study underscores the danger associated with the inhalation of ETS in the public bars in Nigeria.

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