OBJECTIVE To investigate the damage effect and mechanisms of cyclophosphamide(CTX)and its active metabolite derivative 4-hydroperoxycyclophosphamide(4-HC)to human neuroblas⁃toma SH-SY5Y cells.METHODS SH-SY5Y cells wer...OBJECTIVE To investigate the damage effect and mechanisms of cyclophosphamide(CTX)and its active metabolite derivative 4-hydroperoxycyclophosphamide(4-HC)to human neuroblas⁃toma SH-SY5Y cells.METHODS SH-SY5Y cells were treated with CTX[0(cell control),0.01,0.1,1,5,10,20,40 and 80 mmol·L^(-1)]and 4-HC[0(cell control),0.01,0.1,1,5,10,20,40 and 80μmol·L^(-1)]for 48 h.Cell confluence and morphology were observed by the IncuCyte ZOOM system.Cell viability was assessed by CCK-8 assay.Lactate dehydrogenase(LDH)release was measured by LDH assay kit.SH-SY5Y cells were treated with CTX(0,1,5,10 and 20 mmol·L^(-1))and 4-HC(0,1,5,10 and 20μmol·L^(-1))for 48 h before cell proliferation was analyzed by 5-ethynyl-2′-deoxyuridine(EdU)staining assay.Immunofluorescence was employed to assess the levels of the DNA double-strand break markerγ-H2AX and to evaluate changes in mitochondrial membrane potential.SH-SY5Y cells were treated with CTX(0,1,5 and 10 mmol·L^(-1))and 4-HC(0,1,5 and 10μmol·L^(-1))for 48 h,and the alterations in glycolysis and oxidative phosphorylation levels were analyzed using the Seahorse XFe96 Analyzer.RESULTS Compared with the cell control group,cell confluence and cell viability were significantly reduced in the CTX and 4-HC groups(P<0.01),and the half-maximal inhibitory concentrations(IC50)for CTX and 4-HC were 4.44 mmol·L^(-1) and 4.78μmol·L^(-1),respectively.The release rate of LDH was signif⁃icantly increased while the percentage of EdU+cells was significantly reduced in the CTX and 4-HC groups(P<0.01).The percentage ofγ-H2AX+cells was significantly increased and mitochondrial membrane potential significantly decreased in the CTX and 4-HC group(P<0.05).Treatment with CTX and 4-HC resulted in reduced levels of maximum glycolytic capacity,glycolytic reserve,maximal respi⁃ration,and ATP production(P<0.05).CONCLUSION CTX and 4-HC exert significant cytotoxic effects on SH-SY5Y cells by disrupting cell membrane structure,impeding cell proliferation,and reducing cell viability.The mechanisms underlying these effects may involve intracellular DNA damage,disturbance of energy metabolism and mitochondrial dysfunction.展开更多
CeTiOx and CeZrTiOx catalysts were prepared by a coprecipitation method and used for selective catalytic reduction of NOx by NH3 （NH3‐SCR）. Various amounts of KNO3 were impregnated on the catalyst surface to invest...CeTiOx and CeZrTiOx catalysts were prepared by a coprecipitation method and used for selective catalytic reduction of NOx by NH3 （NH3‐SCR）. Various amounts of KNO3 were impregnated on the catalyst surface to investigate the effects of Zr addition on the K＋‐poisoning resistance of the CeTiOx catalyst. The NH3‐SCR performance of the catalysts showed that the NOx removal activity of the Zr‐modified catalyst after poisoning was better than that of the CeTiOx catalyst. Brunau‐er‐Emmett‐Teller data indicated that the Zr‐containing catalyst had a larger specific surface area and pore volume both before and after K＋poisoning. X‐ray diffraction, Raman spectroscopy, and transmission electron microscopy showed that Zr doping inhibited anatase TiO2 crystal grain growth, i.e., the molten salt flux effect caused by the loaded KNO3 was inhibited. The Ce 3d X‐ray photoelectron spectra showed that the Ce3＋/Ce4＋ratio of CeZrTiOx decreased more slowly than that of CeTiOx with increasing K＋loading, indicating that Zr addition preserved more crystal defects and oxygen vacancies; this improved the catalytic performance. The acidity was a key factor in the NH3‐SCR performance; the temperature‐programmed desorption of NH3 results showed that Zr doping inhibited the decrease in the surface acidity. The results suggest that Zr improved the K＋‐poisoning resistance of the CeTiOx catalyst.展开更多
The effect of inhaled nano-TiO2 on lung histology and serum biochemical indexes is evaluated in healthy and adult Kunming mice（eight in each group）after exposure to TiO2 aerosols（1 500 mg/m3）in a sealed chamber.An...The effect of inhaled nano-TiO2 on lung histology and serum biochemical indexes is evaluated in healthy and adult Kunming mice（eight in each group）after exposure to TiO2 aerosols（1 500 mg/m3）in a sealed chamber.Another eight mice are exposed to indoor air to be served as a control group.Lung tissue and blood are collected after euthanizing the animals.The results show that lactate dehydrogenase（LDH）activity increases in all experimental groups.Alanine aminotransferase（ALT）activity and blood urea nitrogen（BUN）levels are increased in the group exposed to TiO2 aerosols for 28 d,and creatinine（Cr）levels are increased in 14 d and 28 d samples（P0.05）.No obvious changes are observed in other serum indexes.Lungs of mice exposed to 28 d exposure show significant but moderate increase in pulmonary inflammation,and many TiO2 particles are found in the interstitium of pulmonary alveoli.展开更多
In this study, the bioaccumulation and toxicity of neodymium （Nd） in pla-narian Dugesia japonica were investigated. The results showed that with the in-creasing dietary Nd supplementation, the concentration of Nd in...In this study, the bioaccumulation and toxicity of neodymium （Nd） in pla-narian Dugesia japonica were investigated. The results showed that with the in-creasing dietary Nd supplementation, the concentration of Nd in the planarian showed a significant linear increase and the balance of mineral elements was bro-ken with the decrease of Ca, Fe and Mo, and the increase of K and Mg. The content of soluble proteins and the activities of superoxide dismutase （SOD） and catalase （CAT） decreased with the increase of Nd concentration, while the content of H2O2 rose gradual y. The mortality was directly proportional to the Nd concentra-tion. The results indicated that planarian is a very sensitive aquatic animal to Nd contamination and can be an indicator organism for Nd pol ution.展开更多
AIM： To evaluate the protective effect of 2′-p-hydroxy benzoylmussaenosidic acid [negundoside （NG）, against carbon tetrachloride （CCl4）-induced toxicity in HUH-7 cel Is.METHODS： CCI4 is a well characterized hep...AIM： To evaluate the protective effect of 2′-p-hydroxy benzoylmussaenosidic acid [negundoside （NG）, against carbon tetrachloride （CCl4）-induced toxicity in HUH-7 cel Is.METHODS： CCI4 is a well characterized hepatotoxin, and inducer of cytochrome P450 2E1 （CYP2E1）-mediated oxidative stress. In addition, lipid peroxidation and accumulation of intracellular calcium are important steps in the pathway involved in CCl4 toxicity. Liver cells （HUH-7） were treated with CCI4, and the mechanism of the cytoprotective effect of NG was assessed. Silymarin, a known hepatoprotective drug, was used as control. RESULTS： NG protected HUH-7 cells against CCl4 toxicity and loss of viability without modulating CYP2E1 activity. Prevention of CCl4 toxicity was associated with a reduction in oxidative damage as reflected by decreased generation of reactive oxygen species （ROS）, a decrease in lipid peroxidation and accumulation of intracellular Ca^2＋ levels and maintenance of intracellular glutathione homeostasis. Decreased mitochondrial membrane potential （MMP）, induction of caspases mediated DNA fragmentation and cell cycle arrest, as a result of CCl4 treatment, were also blocked by NG. The protection afforded by NG seemed to be mediated by activation of cyclic adenosine monophosphate （cAMP） synthesis and inhibition of phospholipases （cPLA2）. CONCLUSION： NG exerts a protective effect on CYP2E1-dependent CCl4 toxicity via inhibition of lipid peroxidation, followed by an improved intracellular calcium homeostasis and inhibition of Ca^2＋-dependent proteases.展开更多
Glucose homeostasis deficiency leads to a chronic increase in blood glucose concentration. In contrast to physiological glucose concentration, chronic super-physiological glucose concentration negatively affects a lar...Glucose homeostasis deficiency leads to a chronic increase in blood glucose concentration. In contrast to physiological glucose concentration, chronic super-physiological glucose concentration negatively affects a large number of organs and tissues. Glucose toxicity means a decrease in insulin secretion and an increase in insulin resistance due to chronic hyperglycemia. It is now generally accepted that glucose toxicity is involved in the worsening of diabetes by affecting the secretion of B-cells. Several mechanisms have been proposed to explain the adverse effects of hyperglycemia. It was found that persistent hyperglycemia caused the functional decline of neutrophils. Infection is thus the main problem resulting from glucose toxicity in the acute phase. In other words, continued hyperglycemia is a life-threatening risk factor, not only in the chronic but also the acute phase, and it becomes a risk factor for infection, particularly in the perioperative period.展开更多
A series of batch experiments were conducted in 125 mL serum bottles to assess the toxicity of different concentrations of ammonia nitrogen to the specific methanogenic activity of anaerobic granular sludge from upflo...A series of batch experiments were conducted in 125 mL serum bottles to assess the toxicity of different concentrations of ammonia nitrogen to the specific methanogenic activity of anaerobic granular sludge from upflow anaerobic sludge bed（UASB） and expanded granular sludge bed（EGSB） reactors. The effects of pH value and temperature on toxicity of ammonia nitrogen to anaerobes were investigated. The results show that the specific methanogenic activity of anaerobic granular sludge suffers inhibition from ammonia nitrogen, the concentrations of ammonia nitrogen that produce 50 % inhibition of specific methanogenic activity for sludge from UASB and EGSB reactor are 2.35 and 2.75 g/L, respectively. Hydrogen utilizing methanogens suffers less inhibition from ammonia mtrogen than that of acetate utilizing methanogens. Hydrogen-producing acetogens that utilize propionate and butyrate as substrates suffer serious inhibition from ammonia nitrogen. The toxicity of ammonia nitrogen to anaerobic granular sludge enhances when pH value and temperature increase. Anaerobic granular sludge can bear higher concentrations of ammonia nitrogen after being acclimated by ammonia nitrogen for 7 d.展开更多
In this study, the O3/BAC/TiO2 catalytic method was used to treat the phenolic wastewater. During the experiments the effects of initial phenol concentration, ozone concentration, pH value, catalyst and other conditio...In this study, the O3/BAC/TiO2 catalytic method was used to treat the phenolic wastewater. During the experiments the effects of initial phenol concentration, ozone concentration, pH value, catalyst and other conditions on the phenol removal rate were investigated. The test results showed that when the phenol concentration was 0.1 g/L, the ozone-containing air flow rate was 0.05 m3/b, the ozone concentration was 3.58 mg/L, the pH value was 7.5, and the treating time was 30 minutes, the phenol removal rate reached 99%, with the COD removal rate equating to 55%. The property of treated wastewater could comply with the first-grade effluent specified in ＂Comprehensive Wastewater Discharge Standard＂ （GB8978--1996）.展开更多
Hydrogen will be at the basis of the World’s energy policy in forthcoming decades, owing to its decarbonized nature, at least when produced from renewables. For now, hydrogen is still essentially produced from fossil...Hydrogen will be at the basis of the World’s energy policy in forthcoming decades, owing to its decarbonized nature, at least when produced from renewables. For now, hydrogen is still essentially produced from fossil feedstock(and to a minor extent from biomass);in consequence the present hydrogen gas on the market is containing non-negligible amounts of impurities that prevent its immediate usage in specialty chemistry or as an energy carrier in fuel cells, e.g. in transportation applications(cars, buses, trains, boats, etc.) that gradually spread on the planet. For these purposes, hydrogen must be of sufficient purity but also sufficiently compressed(at high pressures, typically 70 MPa), rendering purification and compression steps unavoidable in the hydrogen cycle. As shown in the first part of this contribution "Electrochemical hydrogen compression and purification versus competing technologies: Part I. pros and cons", electrochemical hydrogen compressors(EHCs), which enable both hydrogen purification and compression, exhibit many theoretical(thermodynamic) and practical(kinetics) advantages over their mechanical counterparts. However, in order to be competitive, EHCs must operate in very intensive conditions(high current density and low cell voltage) that can only be reached if their core materials, e.g. the membrane and the electrodes/electrocatalysts, are optimized. This contribution will particularly focus on the properties electrocatalysts must exhibit to be used in EHCs: they shall promote(very) fast hydrogen oxidation reaction(HOR) in presence of impurities, which implies that they are(very) tolerant to poisons as well. This consists of a prerequisite for the operation of the anode of an EHC used for the purification-compression of hydrogen, and the materials developed for poison-tolerance in the vast literature on low-temperature fuel cells, may not always satisfy these two criteria, as this contribution will review.展开更多
Acute toxicity and accumulated toxicity of chlorine dioxide (ClO2) and by-products chlorite (ClO2-) and chlorate (ClO3-) in water acted on mice are studied by the method of Horn and accumulation coefficient. Subchroni...Acute toxicity and accumulated toxicity of chlorine dioxide (ClO2) and by-products chlorite (ClO2-) and chlorate (ClO3-) in water acted on mice are studied by the method of Horn and accumulation coefficient. Subchronic toxicity of the mixture of ClO2 and ClO2-and ClO3- in water acted on rat is studied though feeding test for 90 days, including statistical analysis of variance on weight gaining, food utilization efficiency,index of blood and serum,liver (or kidney) to body weight ratio, and histopathological examination on liver and kidney. The results show that aqueous solution of ClO2, NaClO2 and NaClO3 ( with the concentration of 276.5 mg/L, 200 mg/L and 200 mg/L respectively) and the mixed aqueous solution of ClO2 with the concentration of 553 mg/L are actually non-poisonous , and non-cumulative aqueous solution as well.展开更多
AIM： To observe the relationship between ethanol-induced oxidative damage in human primary cultured hepatocytes and cytochrome P450 2E1 （CYP2E1） activity, in order to address if inhibition of CYP2E1 could attenuate...AIM： To observe the relationship between ethanol-induced oxidative damage in human primary cultured hepatocytes and cytochrome P450 2E1 （CYP2E1） activity, in order to address if inhibition of CYP2E1 could attenuate ethanol- induced cellular damage. METHODS： The dose-dependent （25-100 mmol/L） and time-dependent （0-24 h） exposures of primary human cultured hepatocytes to ethanol were carried out. CYP2E1 activity and protein expression were detected by spectrophotometer and Western blot analysis respectively. Hepatotoxicity was investigated by determination of lactate dehydrogenase （LDH） and aspartate transaminase （AST） level in hepatocyte culture supernatants, as well as the intracellular formation of malondialdehyde （MDA）. RESULTS： A dose-and time-dependent response between ethanol exposure and CYP2E1 activity in human hepatocytes was demonstrated. Moreover, there was a time-dependent increase of CYP2E1 protein after 100 mmol/L ethanol exposure. Meanwhile, ethanol exposure of hepatocytes caused a time-dependent increase of cellular MDA level, LDH, and AST activities in supernatants. Furthermore, the inhibitor of CYP2E1, diallyl sulfide （DAS） could partly attenuate the increases of MDA, LDH, and AST in human hepatocytes. CONCLUSION： A positive relationship between ethanolinduced oxidative damage in human primary cultured hepatocytes and CYP2E1 activity was exhibited, and the inhibition of CYP2E1 could partly attenuate ethanol-induced oxidative damage.展开更多
Several studies have characterized the cellular and molecular mechanisms of hepatocyte injury caused by the retention of hydrophobic bile acids （BAs） in cholestatic diseases. BAs may disrupt cell membranes through t...Several studies have characterized the cellular and molecular mechanisms of hepatocyte injury caused by the retention of hydrophobic bile acids （BAs） in cholestatic diseases. BAs may disrupt cell membranes through their detergent action on lipid components and can promote the generation of reactive oxygen species that, in turn, oxidatively modify lipids, proteins, and nucleic acids, and eventually cause hepatocyte necrosis and apoptosis. Several pathways are involved in triggering hepatocyte apoptosis. Toxic BAs can activate hepatocyte death receptors directly and induce oxidative damage, thereby causing mitochondrial dysfunction, and induce endoplasmic reticulum stress. When these compounds are taken up and accumulate inside biliary cells, they can also cause apoptosis. Regarding extrahepatic tissues, the accumulation of BAs in the systemic circulation may contribute to endothelial injury in the kidney and lungs. In gastrointestinal cells, BAs may behave as cancer promoters through an indirect mechanism involving oxidative stress and DNA damage, as well as acting as selection agents for apoptosis-resistant cells. The accumulation of BAs may have also deleterious effects on placental and fetal cells. However, other BAs, such as ursodeoxycholic acid, have been shown to modulate BA-induced injury in hepatocytes. The major beneficial effects of treatment with ursodeoxycholic acid are protection against cytotoxicity due to more toxic BAs; the stimulation of hepatobiliary secretion; antioxidant activity, due in part to an enhancement in glutathione levels; and the inhibition of liver cell apoptosis. Other natural BAs or their derivatives, such as cholyI-N- methylglycine or pharmacological properties. cholylsarcosine, interest owing have also aroused to their protective展开更多
AIM: To assess the extent of micronutrient and oxidative stress in blood and to examine their linkages with viral loads in chronic hepatitis C patients.METHODS: Hepatitis C virus (HCV)-RNA levels were quantified in th...AIM: To assess the extent of micronutrient and oxidative stress in blood and to examine their linkages with viral loads in chronic hepatitis C patients.METHODS: Hepatitis C virus (HCV)-RNA levels were quantified in the serum from 37 previously untreated patients with chronic hepatitis C. The plasma and erythrocyte micronutrients (zinc, selenium, copper, and iron) were estimated, and malondialdehyde (MDA)contents were determined as a marker to detect oxidative stress. Antioxidant enzymes, superoxide dismutase (SOD),glutathione peroxidase (GPX) and glutathione reductase (GR) activities in blood were also measured. The control group contained 31 healthy volunteers.RESULTS: The contents of zinc (Zn), and selenium (Se)in plasma and erythrocytes were significantly lower in hepatitis C patients than in the controls. On the contrary,copper (Cu) levels were significantly higher. Furthermore,plasma and erythrocyte MDA levels, and the SOD and GR activities in erythrocytes significantly increased in hepatitis C patients compared to the controls. However, the plasma GPX activity in patients was markedly lower. Plasma Se (r= -0.730, P<0.05), Cu (r = 0.635), and GPX (r = -0.675)demonstrated correlations with HCV-RNA loads. Significant correlation coefficients were also observed between HCV-RNA levels and erythrocyte Zn (r = -0.403), Se (r = -0.544), Cu (r = 0.701) and MDA (r = 0.629) and GR (r = 0.441).CONCLUSION: The levels of Zn, Se, Cu, and oxidative stress (MDA), as well as related anti-oxidative enzymes (GR and GPX) in blood have important impact on the viral factors in chronic hepatitis C. The distribution of these parameters might be significant biomarkers for HCV.展开更多
Objective：To explore the protective effect of sound preconditioning against ototoxicity induced by cisplatin and its possible mechanism with respect to the nitric oxide （NO） pathway. Methods： Albino guinea pigs we...Objective：To explore the protective effect of sound preconditioning against ototoxicity induced by cisplatin and its possible mechanism with respect to the nitric oxide （NO） pathway. Methods： Albino guinea pigs were divided into silent control, CDDP,sound preconditioning and sound preconditioning＋CDDP groups. The animals of the CDDP group were injected with cisplatin intravenously 8 mg/kg b.w. The animals in the sound preconditioning were exposed to white noise at 85dB SPL, 5h/d, for 10 d （sound preconditioning）. The animals in the sound preconditioning＋CDDP group were treated with sound preconditioning first and then administrated with cisplatin intravenously 8 mg/kg b.w. Hearing thresholds of auditory brainstem responses （ABRs） of all animals were measured to evaluate hearing function. Hair cell loss was estimated via surface preparation. Cochlear tissue was assayed for measurement of NO level and immunohistochemistry method was used for inducible nitric oxide synthase （iNOS） analysis. Results： There was no significant difference between the silent control and sound preconditioning animals with respect to either functional or histological measures. Among the animals in the CDDP group, there was a significant elevation of threshold at the high test frequencies after administration compared with the silent control group （P〈0. 05）. Morphological examination showed that there was obvious loss of the OHC, especially in the third row of the basal turn. The NO level and immunoreactivity to iNOS in this group were higher and more intensive than those of the silent control group （P〈0. 05）. The ABR thresholds in the sound preconditioning ＋ CDDP group were much lower than those of the CDDP group （P〈0.05）. Slight sporadic loss of OHC was found in this group. The immunoreactivity to iNOS and the level of NO in cochlea decreased significantly compared with the CDDP group （P〈 0. 05）. Conclusion： It is suggested that sound preconditioning, to some extent, provides protective effect against ototoxicity of cisplatin. The excess synthesis of NO induced by the over-expressed of iNOS may be involved in the CDDP induced ototoxicity. The possible mechanism is related to suppression of the NO pathway.展开更多
The effect of molybdenum oxide on the activity and durability of Ce O2-Ti O2 catalyst for NO reduction by NH3 was examined. It was found that the introduction of Mo could improve the low-temperature NH3-SCR activity a...The effect of molybdenum oxide on the activity and durability of Ce O2-Ti O2 catalyst for NO reduction by NH3 was examined. It was found that the introduction of Mo could improve the low-temperature NH3-SCR activity and SO2/H2 O durability of the Ce O2-Ti O2 catalyst and an optimal loading of Mo was 4?wt.%. The best Mo O3/Ce O2-Ti O2 catalyst displayed over 90% NO conversion from 200 °C to 400 °C and obtained 4-fold increase in NO conversion compared to Ce O2-Ti O2 at 150 °C. The characterization results revealed that the number of Br?nsted acid sites over Mo O3/Ce O2-Ti O2 was significantly increased, and the adsorption of nitrate species was dramatically weakened because of the coverage of Mo O3, which were favorable for the high NH3-SCR performance. It is believed that the Mo O3/Ce O2-Ti O2 catalyst is a suitable substitute for the NH3-SCR reaction.展开更多
文摘OBJECTIVE To investigate the damage effect and mechanisms of cyclophosphamide(CTX)and its active metabolite derivative 4-hydroperoxycyclophosphamide(4-HC)to human neuroblas⁃toma SH-SY5Y cells.METHODS SH-SY5Y cells were treated with CTX[0(cell control),0.01,0.1,1,5,10,20,40 and 80 mmol·L^(-1)]and 4-HC[0(cell control),0.01,0.1,1,5,10,20,40 and 80μmol·L^(-1)]for 48 h.Cell confluence and morphology were observed by the IncuCyte ZOOM system.Cell viability was assessed by CCK-8 assay.Lactate dehydrogenase(LDH)release was measured by LDH assay kit.SH-SY5Y cells were treated with CTX(0,1,5,10 and 20 mmol·L^(-1))and 4-HC(0,1,5,10 and 20μmol·L^(-1))for 48 h before cell proliferation was analyzed by 5-ethynyl-2′-deoxyuridine(EdU)staining assay.Immunofluorescence was employed to assess the levels of the DNA double-strand break markerγ-H2AX and to evaluate changes in mitochondrial membrane potential.SH-SY5Y cells were treated with CTX(0,1,5 and 10 mmol·L^(-1))and 4-HC(0,1,5 and 10μmol·L^(-1))for 48 h,and the alterations in glycolysis and oxidative phosphorylation levels were analyzed using the Seahorse XFe96 Analyzer.RESULTS Compared with the cell control group,cell confluence and cell viability were significantly reduced in the CTX and 4-HC groups(P<0.01),and the half-maximal inhibitory concentrations(IC50)for CTX and 4-HC were 4.44 mmol·L^(-1) and 4.78μmol·L^(-1),respectively.The release rate of LDH was signif⁃icantly increased while the percentage of EdU+cells was significantly reduced in the CTX and 4-HC groups(P<0.01).The percentage ofγ-H2AX+cells was significantly increased and mitochondrial membrane potential significantly decreased in the CTX and 4-HC group(P<0.05).Treatment with CTX and 4-HC resulted in reduced levels of maximum glycolytic capacity,glycolytic reserve,maximal respi⁃ration,and ATP production(P<0.05).CONCLUSION CTX and 4-HC exert significant cytotoxic effects on SH-SY5Y cells by disrupting cell membrane structure,impeding cell proliferation,and reducing cell viability.The mechanisms underlying these effects may involve intracellular DNA damage,disturbance of energy metabolism and mitochondrial dysfunction.
基金supported by the Major Research Program of Sichuan Province Science and Technology Department (2012FZ0008)the National Natural Science Foundation of China (21173153)+1 种基金the National High Technology Research and Development Program of China (863 Program,2013AA065304)the Sichuan University Research Foundation for Young Teachers (2015SCU11056)~~
文摘CeTiOx and CeZrTiOx catalysts were prepared by a coprecipitation method and used for selective catalytic reduction of NOx by NH3 （NH3‐SCR）. Various amounts of KNO3 were impregnated on the catalyst surface to investigate the effects of Zr addition on the K＋‐poisoning resistance of the CeTiOx catalyst. The NH3‐SCR performance of the catalysts showed that the NOx removal activity of the Zr‐modified catalyst after poisoning was better than that of the CeTiOx catalyst. Brunau‐er‐Emmett‐Teller data indicated that the Zr‐containing catalyst had a larger specific surface area and pore volume both before and after K＋poisoning. X‐ray diffraction, Raman spectroscopy, and transmission electron microscopy showed that Zr doping inhibited anatase TiO2 crystal grain growth, i.e., the molten salt flux effect caused by the loaded KNO3 was inhibited. The Ce 3d X‐ray photoelectron spectra showed that the Ce3＋/Ce4＋ratio of CeZrTiOx decreased more slowly than that of CeTiOx with increasing K＋loading, indicating that Zr addition preserved more crystal defects and oxygen vacancies; this improved the catalytic performance. The acidity was a key factor in the NH3‐SCR performance; the temperature‐programmed desorption of NH3 results showed that Zr doping inhibited the decrease in the surface acidity. The results suggest that Zr improved the K＋‐poisoning resistance of the CeTiOx catalyst.
文摘The effect of inhaled nano-TiO2 on lung histology and serum biochemical indexes is evaluated in healthy and adult Kunming mice（eight in each group）after exposure to TiO2 aerosols（1 500 mg/m3）in a sealed chamber.Another eight mice are exposed to indoor air to be served as a control group.Lung tissue and blood are collected after euthanizing the animals.The results show that lactate dehydrogenase（LDH）activity increases in all experimental groups.Alanine aminotransferase（ALT）activity and blood urea nitrogen（BUN）levels are increased in the group exposed to TiO2 aerosols for 28 d,and creatinine（Cr）levels are increased in 14 d and 28 d samples（P0.05）.No obvious changes are observed in other serum indexes.Lungs of mice exposed to 28 d exposure show significant but moderate increase in pulmonary inflammation,and many TiO2 particles are found in the interstitium of pulmonary alveoli.
基金Supported by Department of Environmental Protection--Special Funds for Biological Diversity Conservation(2111101)National Natural Science Foundation of China(30900071)Start-Up Funding for PhD Research at Shandong University of Technology(4041-406027)~~
文摘In this study, the bioaccumulation and toxicity of neodymium （Nd） in pla-narian Dugesia japonica were investigated. The results showed that with the in-creasing dietary Nd supplementation, the concentration of Nd in the planarian showed a significant linear increase and the balance of mineral elements was bro-ken with the decrease of Ca, Fe and Mo, and the increase of K and Mg. The content of soluble proteins and the activities of superoxide dismutase （SOD） and catalase （CAT） decreased with the increase of Nd concentration, while the content of H2O2 rose gradual y. The mortality was directly proportional to the Nd concentra-tion. The results indicated that planarian is a very sensitive aquatic animal to Nd contamination and can be an indicator organism for Nd pol ution.
基金Indian Institute of Integrative Medicine, Council of Scientific and Industrial Research
文摘AIM： To evaluate the protective effect of 2′-p-hydroxy benzoylmussaenosidic acid [negundoside （NG）, against carbon tetrachloride （CCl4）-induced toxicity in HUH-7 cel Is.METHODS： CCI4 is a well characterized hepatotoxin, and inducer of cytochrome P450 2E1 （CYP2E1）-mediated oxidative stress. In addition, lipid peroxidation and accumulation of intracellular calcium are important steps in the pathway involved in CCl4 toxicity. Liver cells （HUH-7） were treated with CCI4, and the mechanism of the cytoprotective effect of NG was assessed. Silymarin, a known hepatoprotective drug, was used as control. RESULTS： NG protected HUH-7 cells against CCl4 toxicity and loss of viability without modulating CYP2E1 activity. Prevention of CCl4 toxicity was associated with a reduction in oxidative damage as reflected by decreased generation of reactive oxygen species （ROS）, a decrease in lipid peroxidation and accumulation of intracellular Ca^2＋ levels and maintenance of intracellular glutathione homeostasis. Decreased mitochondrial membrane potential （MMP）, induction of caspases mediated DNA fragmentation and cell cycle arrest, as a result of CCl4 treatment, were also blocked by NG. The protection afforded by NG seemed to be mediated by activation of cyclic adenosine monophosphate （cAMP） synthesis and inhibition of phospholipases （cPLA2）. CONCLUSION： NG exerts a protective effect on CYP2E1-dependent CCl4 toxicity via inhibition of lipid peroxidation, followed by an improved intracellular calcium homeostasis and inhibition of Ca^2＋-dependent proteases.
文摘Glucose homeostasis deficiency leads to a chronic increase in blood glucose concentration. In contrast to physiological glucose concentration, chronic super-physiological glucose concentration negatively affects a large number of organs and tissues. Glucose toxicity means a decrease in insulin secretion and an increase in insulin resistance due to chronic hyperglycemia. It is now generally accepted that glucose toxicity is involved in the worsening of diabetes by affecting the secretion of B-cells. Several mechanisms have been proposed to explain the adverse effects of hyperglycemia. It was found that persistent hyperglycemia caused the functional decline of neutrophils. Infection is thus the main problem resulting from glucose toxicity in the acute phase. In other words, continued hyperglycemia is a life-threatening risk factor, not only in the chronic but also the acute phase, and it becomes a risk factor for infection, particularly in the perioperative period.
文摘A series of batch experiments were conducted in 125 mL serum bottles to assess the toxicity of different concentrations of ammonia nitrogen to the specific methanogenic activity of anaerobic granular sludge from upflow anaerobic sludge bed（UASB） and expanded granular sludge bed（EGSB） reactors. The effects of pH value and temperature on toxicity of ammonia nitrogen to anaerobes were investigated. The results show that the specific methanogenic activity of anaerobic granular sludge suffers inhibition from ammonia nitrogen, the concentrations of ammonia nitrogen that produce 50 % inhibition of specific methanogenic activity for sludge from UASB and EGSB reactor are 2.35 and 2.75 g/L, respectively. Hydrogen utilizing methanogens suffers less inhibition from ammonia mtrogen than that of acetate utilizing methanogens. Hydrogen-producing acetogens that utilize propionate and butyrate as substrates suffer serious inhibition from ammonia nitrogen. The toxicity of ammonia nitrogen to anaerobic granular sludge enhances when pH value and temperature increase. Anaerobic granular sludge can bear higher concentrations of ammonia nitrogen after being acclimated by ammonia nitrogen for 7 d.
文摘In this study, the O3/BAC/TiO2 catalytic method was used to treat the phenolic wastewater. During the experiments the effects of initial phenol concentration, ozone concentration, pH value, catalyst and other conditions on the phenol removal rate were investigated. The test results showed that when the phenol concentration was 0.1 g/L, the ozone-containing air flow rate was 0.05 m3/b, the ozone concentration was 3.58 mg/L, the pH value was 7.5, and the treating time was 30 minutes, the phenol removal rate reached 99%, with the COD removal rate equating to 55%. The property of treated wastewater could comply with the first-grade effluent specified in ＂Comprehensive Wastewater Discharge Standard＂ （GB8978--1996）.
基金The authors thank the Auvergne Rhone-Alpes region for the funding of the PhD thesis of Marine TregaroPart of the work has been performed within the framework of the Centre of Excellence of Multifunctional Architectured Materials“CEMAM”no.ANR-10-LABX-44-01Both MT and MR make their PhD in the frame of the Eco-Sesa project,funded by IDEX Universite Grenoble Alpes.
文摘Hydrogen will be at the basis of the World’s energy policy in forthcoming decades, owing to its decarbonized nature, at least when produced from renewables. For now, hydrogen is still essentially produced from fossil feedstock(and to a minor extent from biomass);in consequence the present hydrogen gas on the market is containing non-negligible amounts of impurities that prevent its immediate usage in specialty chemistry or as an energy carrier in fuel cells, e.g. in transportation applications(cars, buses, trains, boats, etc.) that gradually spread on the planet. For these purposes, hydrogen must be of sufficient purity but also sufficiently compressed(at high pressures, typically 70 MPa), rendering purification and compression steps unavoidable in the hydrogen cycle. As shown in the first part of this contribution "Electrochemical hydrogen compression and purification versus competing technologies: Part I. pros and cons", electrochemical hydrogen compressors(EHCs), which enable both hydrogen purification and compression, exhibit many theoretical(thermodynamic) and practical(kinetics) advantages over their mechanical counterparts. However, in order to be competitive, EHCs must operate in very intensive conditions(high current density and low cell voltage) that can only be reached if their core materials, e.g. the membrane and the electrodes/electrocatalysts, are optimized. This contribution will particularly focus on the properties electrocatalysts must exhibit to be used in EHCs: they shall promote(very) fast hydrogen oxidation reaction(HOR) in presence of impurities, which implies that they are(very) tolerant to poisons as well. This consists of a prerequisite for the operation of the anode of an EHC used for the purification-compression of hydrogen, and the materials developed for poison-tolerance in the vast literature on low-temperature fuel cells, may not always satisfy these two criteria, as this contribution will review.
文摘Acute toxicity and accumulated toxicity of chlorine dioxide (ClO2) and by-products chlorite (ClO2-) and chlorate (ClO3-) in water acted on mice are studied by the method of Horn and accumulation coefficient. Subchronic toxicity of the mixture of ClO2 and ClO2-and ClO3- in water acted on rat is studied though feeding test for 90 days, including statistical analysis of variance on weight gaining, food utilization efficiency,index of blood and serum,liver (or kidney) to body weight ratio, and histopathological examination on liver and kidney. The results show that aqueous solution of ClO2, NaClO2 and NaClO3 ( with the concentration of 276.5 mg/L, 200 mg/L and 200 mg/L respectively) and the mixed aqueous solution of ClO2 with the concentration of 553 mg/L are actually non-poisonous , and non-cumulative aqueous solution as well.
基金Supported by the National Science Foundation of China, No. 30271130
文摘AIM： To observe the relationship between ethanol-induced oxidative damage in human primary cultured hepatocytes and cytochrome P450 2E1 （CYP2E1） activity, in order to address if inhibition of CYP2E1 could attenuate ethanol- induced cellular damage. METHODS： The dose-dependent （25-100 mmol/L） and time-dependent （0-24 h） exposures of primary human cultured hepatocytes to ethanol were carried out. CYP2E1 activity and protein expression were detected by spectrophotometer and Western blot analysis respectively. Hepatotoxicity was investigated by determination of lactate dehydrogenase （LDH） and aspartate transaminase （AST） level in hepatocyte culture supernatants, as well as the intracellular formation of malondialdehyde （MDA）. RESULTS： A dose-and time-dependent response between ethanol exposure and CYP2E1 activity in human hepatocytes was demonstrated. Moreover, there was a time-dependent increase of CYP2E1 protein after 100 mmol/L ethanol exposure. Meanwhile, ethanol exposure of hepatocytes caused a time-dependent increase of cellular MDA level, LDH, and AST activities in supernatants. Furthermore, the inhibitor of CYP2E1, diallyl sulfide （DAS） could partly attenuate the increases of MDA, LDH, and AST in human hepatocytes. CONCLUSION： A positive relationship between ethanolinduced oxidative damage in human primary cultured hepatocytes and CYP2E1 activity was exhibited, and the inhibition of CYP2E1 could partly attenuate ethanol-induced oxidative damage.
基金Supported by Instituto de Salud CarlosTM,FIS, Spain (GrantsPI070517 and PI080151)Fundacion Investigacion Medica Mutua Madrilea, Spain (Conv-TM,, 2006)+3 种基金Junta de Castillay Leon, Spain (Grants GR75-2008, SA033A08, SA03508 and SA03608)Ministerio de Ciencia y Tecnologia, Plan Nacional de Investigacion Cientifi ca, Desarrollo e Innovacion Tecnologica, Spain (Grant BFU2006-12577)The group is member of the Network for Cooperative Research on Membrane Transport Proteins (REIT), co-funded by the Ministerio de Educacion y Ciencia, Spain, and the European Regional Development Fund (ERDF) (Grant BFU2007-30688-E/BFI)belongs to the CIBERehd (Centro de Investigacion Biomedica en Red para el Estudio de Enfermedades Hepaticas y Digestivas), Instituto de Salud CarlosTM
文摘Several studies have characterized the cellular and molecular mechanisms of hepatocyte injury caused by the retention of hydrophobic bile acids （BAs） in cholestatic diseases. BAs may disrupt cell membranes through their detergent action on lipid components and can promote the generation of reactive oxygen species that, in turn, oxidatively modify lipids, proteins, and nucleic acids, and eventually cause hepatocyte necrosis and apoptosis. Several pathways are involved in triggering hepatocyte apoptosis. Toxic BAs can activate hepatocyte death receptors directly and induce oxidative damage, thereby causing mitochondrial dysfunction, and induce endoplasmic reticulum stress. When these compounds are taken up and accumulate inside biliary cells, they can also cause apoptosis. Regarding extrahepatic tissues, the accumulation of BAs in the systemic circulation may contribute to endothelial injury in the kidney and lungs. In gastrointestinal cells, BAs may behave as cancer promoters through an indirect mechanism involving oxidative stress and DNA damage, as well as acting as selection agents for apoptosis-resistant cells. The accumulation of BAs may have also deleterious effects on placental and fetal cells. However, other BAs, such as ursodeoxycholic acid, have been shown to modulate BA-induced injury in hepatocytes. The major beneficial effects of treatment with ursodeoxycholic acid are protection against cytotoxicity due to more toxic BAs; the stimulation of hepatobiliary secretion; antioxidant activity, due in part to an enhancement in glutathione levels; and the inhibition of liver cell apoptosis. Other natural BAs or their derivatives, such as cholyI-N- methylglycine or pharmacological properties. cholylsarcosine, interest owing have also aroused to their protective
基金Supported by the Kuang-Tien General Hospital, Taichung, Taiwan,China
文摘AIM: To assess the extent of micronutrient and oxidative stress in blood and to examine their linkages with viral loads in chronic hepatitis C patients.METHODS: Hepatitis C virus (HCV)-RNA levels were quantified in the serum from 37 previously untreated patients with chronic hepatitis C. The plasma and erythrocyte micronutrients (zinc, selenium, copper, and iron) were estimated, and malondialdehyde (MDA)contents were determined as a marker to detect oxidative stress. Antioxidant enzymes, superoxide dismutase (SOD),glutathione peroxidase (GPX) and glutathione reductase (GR) activities in blood were also measured. The control group contained 31 healthy volunteers.RESULTS: The contents of zinc (Zn), and selenium (Se)in plasma and erythrocytes were significantly lower in hepatitis C patients than in the controls. On the contrary,copper (Cu) levels were significantly higher. Furthermore,plasma and erythrocyte MDA levels, and the SOD and GR activities in erythrocytes significantly increased in hepatitis C patients compared to the controls. However, the plasma GPX activity in patients was markedly lower. Plasma Se (r= -0.730, P<0.05), Cu (r = 0.635), and GPX (r = -0.675)demonstrated correlations with HCV-RNA loads. Significant correlation coefficients were also observed between HCV-RNA levels and erythrocyte Zn (r = -0.403), Se (r = -0.544), Cu (r = 0.701) and MDA (r = 0.629) and GR (r = 0.441).CONCLUSION: The levels of Zn, Se, Cu, and oxidative stress (MDA), as well as related anti-oxidative enzymes (GR and GPX) in blood have important impact on the viral factors in chronic hepatitis C. The distribution of these parameters might be significant biomarkers for HCV.
基金Supported by National Natural Science Foundation of China(No.30470419)
文摘Objective：To explore the protective effect of sound preconditioning against ototoxicity induced by cisplatin and its possible mechanism with respect to the nitric oxide （NO） pathway. Methods： Albino guinea pigs were divided into silent control, CDDP,sound preconditioning and sound preconditioning＋CDDP groups. The animals of the CDDP group were injected with cisplatin intravenously 8 mg/kg b.w. The animals in the sound preconditioning were exposed to white noise at 85dB SPL, 5h/d, for 10 d （sound preconditioning）. The animals in the sound preconditioning＋CDDP group were treated with sound preconditioning first and then administrated with cisplatin intravenously 8 mg/kg b.w. Hearing thresholds of auditory brainstem responses （ABRs） of all animals were measured to evaluate hearing function. Hair cell loss was estimated via surface preparation. Cochlear tissue was assayed for measurement of NO level and immunohistochemistry method was used for inducible nitric oxide synthase （iNOS） analysis. Results： There was no significant difference between the silent control and sound preconditioning animals with respect to either functional or histological measures. Among the animals in the CDDP group, there was a significant elevation of threshold at the high test frequencies after administration compared with the silent control group （P〈0. 05）. Morphological examination showed that there was obvious loss of the OHC, especially in the third row of the basal turn. The NO level and immunoreactivity to iNOS in this group were higher and more intensive than those of the silent control group （P〈0. 05）. The ABR thresholds in the sound preconditioning ＋ CDDP group were much lower than those of the CDDP group （P〈0.05）. Slight sporadic loss of OHC was found in this group. The immunoreactivity to iNOS and the level of NO in cochlea decreased significantly compared with the CDDP group （P〈 0. 05）. Conclusion： It is suggested that sound preconditioning, to some extent, provides protective effect against ototoxicity of cisplatin. The excess synthesis of NO induced by the over-expressed of iNOS may be involved in the CDDP induced ototoxicity. The possible mechanism is related to suppression of the NO pathway.
基金supported by the National Natural Science Foundation of China(21773106,21707066,21677069,and 21806077)the China Postdoctoral Science Foundation(2018M642206)~~
文摘The effect of molybdenum oxide on the activity and durability of Ce O2-Ti O2 catalyst for NO reduction by NH3 was examined. It was found that the introduction of Mo could improve the low-temperature NH3-SCR activity and SO2/H2 O durability of the Ce O2-Ti O2 catalyst and an optimal loading of Mo was 4?wt.%. The best Mo O3/Ce O2-Ti O2 catalyst displayed over 90% NO conversion from 200 °C to 400 °C and obtained 4-fold increase in NO conversion compared to Ce O2-Ti O2 at 150 °C. The characterization results revealed that the number of Br?nsted acid sites over Mo O3/Ce O2-Ti O2 was significantly increased, and the adsorption of nitrate species was dramatically weakened because of the coverage of Mo O3, which were favorable for the high NH3-SCR performance. It is believed that the Mo O3/Ce O2-Ti O2 catalyst is a suitable substitute for the NH3-SCR reaction.
