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[PMID]: 29293455
[Au] Autor:Chen P; Bornhorst J; Aschner M
[Ad] Address:Department of Molecular Pharmacology, Albert Einstein College of Medicine; 1300 Morris Park Ave, Bronx, NY 11354, USA, pan.chen@einstein.yu.edu.
[Ti] Title:Manganese metabolism in humans.
[So] Source:Front Biosci (Landmark Ed);23:1655-1679, 2018 Mar 01.
[Is] ISSN:1093-4715
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Manganese (Mn) is an essential nutrient for intracellular activities; it functions as a cofactor for a variety of enzymes, including arginase, glutamine synthetase (GS), pyruvate carboxylase and Mn superoxide dismutase (Mn-SOD). Through these metalloproteins, Mn plays critically important roles in development, digestion, reproduction, antioxidant defense, energy production, immune response and regulation of neuronal activities. Mn deficiency is rare. In contrast Mn poisoning may be encountered upon overexposure to this metal. Excessive Mn tends to accumulate in the liver, pancreas, bone, kidney and brain, with the latter being the major target of Mn intoxication. Hepatic cirrhosis, polycythemia, hypermanganesemia, dystonia and Parkinsonism-like symptoms have been reported in patients with Mn poisoning. In recent years, Mn has come to the forefront of environmental concerns due to its neurotoxicity. Molecular mechanisms of Mn toxicity include oxidative stress, mitochondrial dysfunction, protein misfolding, endoplasmic reticulum (ER) stress, autophagy dysregulation, apoptosis, and disruption of other metal homeostasis. The mechanisms of Mn homeostasis are not fully understood. Here, we will address recent progress in Mn absorption, distribution and elimination across different tissues, as well as the intracellular regulation of Mn homeostasis in cells. We will conclude with recommendations for future research areas on Mn metabolism.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180102
[Lr] Last revision date:180102
[St] Status:In-Data-Review

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[PMID]: 29058747
[Au] Autor:Kumar V; Mishra RK; Kaur G; Dutta D
[Ad] Address:CSIR-Institute of Microbial Technology, Sector 39-A, Chandigarh 160036, India. dutta@imtech.res.in.
[Ti] Title:Cobalt and nickel impair DNA metabolism by the oxidative stress independent pathway.
[So] Source:Metallomics;9(11):1596-1609, 2017 Nov 15.
[Is] ISSN:1756-591X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:The oxidative stress that evolves under cobalt and nickel exposure is thought to exert toxicity, though the exact routes of such metal poisoning remain ambiguous. We revisited the metal toxicity in Escherichia coli to show that cobalt and nickel exposure at levels as low as 0.5 and 1 mM, respectively, visibly inhibits growth. We also observed that acidic conditions aggravated, while alkaline conditions alleviated the metal toxicity. Besides, 1 mM manganese, which is non-cytotoxic, as judged by the growth of E. coli, synergistically elevated cobalt and nickel stress. However, the metal toxicity did not lead to oxidative stress in E. coli. On the other hand, we show that cobalt and nickel, but not manganese, reduced the rate of DNA replication to 50% within 2 hours. Interestingly, the metal ions promoted DNA double-strand breaks but did not induce SOS repair pathways, indicating that the metal ions could block SOS induction. To test this, we show that cobalt and nickel, but not manganese, suppressed the nalidixic acid-induced SOS response. Finally, using an in vitro assay system, we demonstrated that cobalt and nickel inhibit RecBCD function, which is essential for SOS induction. Therefore, our data indicate that cobalt and nickel affect DNA replication, damage DNA, and inhibit the SOS repair pathway to exert toxicity.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1710
[Cu] Class update date: 171116
[Lr] Last revision date:171116
[St] Status:In-Process
[do] DOI:10.1039/c7mt00231a

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[PMID]: 28760553
[Au] Autor:Fu XZ; Tong YH; Zhou X; Ling LL; Chun CP; Cao L; Zeng M; Peng LZ
[Ad] Address:Citrus Research Institute, Southwest University, Chongqing 400712, China; Citrus Research Institute, Chinese Academy of Agricultural Sciences, Chongqing 400712, China. Electronic address: fuxingzheng@cric.cn.
[Ti] Title:Genome-wide identification of sweet orange (Citrus sinensis) metal tolerance proteins and analysis of their expression patterns under zinc, manganese, copper, and cadmium toxicity.
[So] Source:Gene;629:1-8, 2017 Sep 20.
[Is] ISSN:1879-0038
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Plant metal tolerance proteins (MTPs) play important roles in heavy metal homeostasis; however, related information in citrus plants is limited. Citrus genome sequencing and assembly have enabled us to perform a systematic analysis of the MTP gene family. We identified 12 MTP genes in sweet orange, which we have named as CitMTP1 and CitMTP3 to CitMTP12 based on their sequence similarity to Arabidopsis thaliana MTPs. The CitMTPs were predicted to encode proteins of 864 to 2556 amino acids in length that included 4 to 6 putative transmembrane domains (TMDs). Furthermore, all the CitMTPs contained a highly conserved signature sequence encompassing the TMD-II and the start of the TMD-III. Phylogenetic analysis further classified the CitMTPs into Fe/Zn-MTP, Mn-MTP, and Zn-MTP subgroups, which coincided with the MTPs of A. thaliana and rice. The closely clustered CitMTPs shared a similar gene structure. Expression analysis indicated that most CitMTP transcripts were upregulated to various extents under heavy metal stress. Among these, CitMTP5 in the roots and CitMTP11 in the leaves during Zn stress, CitMTP8 in the roots and CitMTP8.1 in the leaves during Mn stress, CitMTP12 in the roots and CitMTP1 in the leaves during Cu stress, and CitMTP11 in the roots and CitMTP1 in the leaves during Cd stress showed the highest extent of upregulation. These findings are suggestive of their individual roles in heavy metal detoxification.
[Mh] MeSH terms primary: Cation Transport Proteins/genetics
Citrus sinensis/genetics
Metals, Heavy/toxicity
Plant Proteins/genetics
[Mh] MeSH terms secundary: Amino Acid Sequence
Cation Transport Proteins/chemistry
Cation Transport Proteins/metabolism
Citrus sinensis/drug effects
Gene Expression Regulation, Plant
Heavy Metal Poisoning
Phylogeny
Plant Leaves/genetics
Plant Leaves/metabolism
Plant Proteins/chemistry
Plant Proteins/metabolism
Plant Roots/genetics
Plant Roots/metabolism
Poisoning
Sequence Alignment
Up-Regulation
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Cation Transport Proteins); 0 (Metals, Heavy); 0 (Plant Proteins)
[Em] Entry month:1708
[Cu] Class update date: 171116
[Lr] Last revision date:171116
[Js] Journal subset:IM
[Da] Date of entry for processing:170802
[St] Status:MEDLINE

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[PMID]: 28673426
[Au] Autor:Prego-Faraldo MV; Vieira LR; Eirin-Lopez JM; Méndez J; Guilhermino L
[Ad] Address:CIIMAR/CIMAR - Interdisciplinary Centre of Marine and Environmental Research, Research Group of Ecotoxicology, Stress Ecology and Environmental Health, University of Porto, Porto, Portugal; XENOMAR Group, Department of Cellular and Molecular Biology, University of A Coruña, A Coruña, Spain; Environm
[Ti] Title:Transcriptional and biochemical analysis of antioxidant enzymes in the mussel Mytilus galloprovincialis during experimental exposures to the toxic dinoflagellate Prorocentrum lima.
[So] Source:Mar Environ Res;129:304-315, 2017 Aug.
[Is] ISSN:1879-0291
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:The genotoxic and cytotoxic effects of Diarrhetic Shellfish Poisoning (DSP) toxins have been widely investigated in bivalve molluscs, representing the main vectors of these compounds in the Atlantic coast of Europe. DSP toxins are produced by Harmful Algal Blooms (HABs) of Dinophysis and Prorocentrum dinoflagellates, being subsequently accumulated by marine organisms and biomagnified throughout trophic webs. Yet, bivalves display increased resistance to the harmful effects of these toxins during HAB episodes. While previous reports have suggested that such resilience might be the result of an increased activity in the bivalve antioxidant system, very little is still known about the specific mechanism underlying the protective effect observed in these organisms. The present work aims to fill this gap by studying transcriptional expression levels and biochemical activities of antioxidant enzymes in different tissues the mussel Mytilus galloprovincialis during experimental exposures to DSP toxins produced by the dinoflagellate Prorocentrum lima. Results are consistent with the presence of a compensatory mechanism involving a down-regulation in the expression of specific genes encoding antioxidant enzymes [i.e., SuperOxide Dismutase (SOD) and CATalase (CAT)] which is counterbalanced by the up-regulation of other antioxidant genes such as Glutathione S-Transferase pi-1 (GST-pi) and Selenium-dependent Glutathione PeroXidase (Se-GPx), respectively. Enzymatic activity analyses mirror gene expression results, revealing high antioxidant activity levels (consistent with a protective role for the antioxidant system) along with reduced lipid peroxidation (increasing the defense against oxidative stress).
[Mh] MeSH terms primary: Dinoflagellida/physiology
Harmful Algal Bloom
Marine Toxins/toxicity
Mytilus/physiology
[Mh] MeSH terms secundary: Animals
Catalase/metabolism
Environmental Monitoring
Europe
Glutathione Peroxidase/metabolism
Superoxide Dismutase/metabolism
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Marine Toxins); EC 1.11.1.6 (Catalase); EC 1.11.1.9 (Glutathione Peroxidase); EC 1.15.1.1 (Superoxide Dismutase)
[Em] Entry month:1708
[Cu] Class update date: 170817
[Lr] Last revision date:170817
[Js] Journal subset:IM
[Da] Date of entry for processing:170705
[St] Status:MEDLINE

  5 / 2503 MEDLINE  
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[PMID]: 28666216
[Au] Autor:Li SW; He Y; Zhao HJ; Wang Y; Liu JJ; Shao YZ; Li JL; Sun X; Zhang LN; Xing MW
[Ad] Address:College of Wildlife Resources, Northeast Forestry University, Harbin 150040, People's Republic of China.
[Ti] Title:Assessment of 28 trace elements and 17 amino acid levels in muscular tissues of broiler chicken (Gallus gallus) suffering from arsenic trioxide.
[So] Source:Ecotoxicol Environ Saf;144:430-437, 2017 Oct.
[Is] ISSN:1090-2414
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:The contents of 28 trace elements, 17 amino acid were evaluated in muscular tissues (wings, crureus and pectoralis) of chickens in response to arsenic trioxide (As O ). A total of 200 one-day-old male Hy-line chickens were fed either a commercial diet (C-group) or an As O supplement diet containing 7.5mg/kg (L-group), 15mg/kg (M-group) or 30mg/kg (H-group) As O for 90 days. The elements content was analyzed by inductively coupled plasma mass spectrometry (ICP-MS). Under As O exposure, the concentration of As were elevated 8.87-15.76 fold, 7.93-15.63 fold and 5.94-12.45 fold in wings, crureus and pectoralis compared to the corresponding C-group, respectively. 19 element levels (lithium (Li), magnesium (Mg), aluminum (Al), silicon (Si), kalium (K), vanadium (V), chromium (Cr), manganese (Mn), nickel (Ni), copper (Cu), selenium (Se), strontium (Sr), molybdenum (Mo), cadmium (Cd), tin (Sn), antimony (Sb), barium (Ba), mercury (Hg) and lead (Pb), 9 element levels (K, Co, Ni, Cu, As, Se, Sr, Sn, Ba and Hg) and 4 element levels (Mn, cobalt (Co), As, Sr and Ba) were significantly increased (P < 0.05) in wing, crureus and pectoralis, respectively. 2 element levels (sodium (Na) and zinc (Zn)), 5 element levels (Li, Na, Si, titanium (Ti and Cr), 13 element levels (Li, Na, Mg, K, V, Cr, iron (Fe), Cu, Zn, Mo, Sn, Hg and Pb) were significantly decreased (P < 0.05) in wing muscle, crureus and pectoralis, respectively. Additionally, in crureus and pectoralis, the content of total amino acids (TAA) was no significant alterations in L and M-group and then increased approximately 10.2% and 7.6% in H-group, respectively (P < 0.05). In wings, the level of total amino acids increased approximately 10% in L-group, whereas it showed unchanged in M and H-group compared to the corresponding C-group. We also observed that significantly increased levels of proline, cysteine, aspartic acid, methionine along with decrease in the tyrosine levels in muscular tissues compared to the corresponding C-group. In conclusion, the residual of As in the muscular tissues of chickens were dose-dependent and disrupts trace element homeostasis, amino acids level in muscular tissues of chickens under As O exposure. Additionally, the response (trace elements and amino acids) were different in wing, thigh and pectoral of chick under As O exposure. This study provided references for further study of heavy metal poisoning and may be helpful to understanding the toxicological mechanism of As O exposure in muscular tissues of chickens.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1707
[Cu] Class update date: 170804
[Lr] Last revision date:170804
[St] Status:In-Process

  6 / 2503 MEDLINE  
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[PMID]: 28595959
[Au] Autor:Lee W; Lee Y; Jeong GS; Ku SK; Bae JS
[Ad] Address:College of Pharmacy, CMRI, Research Institute of Pharmaceutical Sciences, BK21 Plus KNU Multi-Omics Based Creative Drug Research Team, Kyungpook National University, Daegu 41566, Republic of Korea.
[Ti] Title:Cudratricusxanthone A attenuates renal injury in septic mice.
[So] Source:Food Chem Toxicol;106(Pt A):404-410, 2017 Aug.
[Is] ISSN:1873-6351
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:As a natural compound extracted from the roots of Cudrania tricuspidata Bureau, Cudratricusxanthone A (CTXA) is known to possess hepatoprotective, anti-inflammatory, and anti-proliferative activities. This study was aimed to clarify the role of CTXA in modulating renal functional damage in a mouse model of sepsis and to elucidate its underlying mechanisms. We examined the renal protective effects of CTXA on cecal ligation and puncture (CLP)-induced renal damage by assessment of serum creatinine, blood urea nitrogen (BUN), lipid peroxidation, total glutathione, glutathione peroxidase activity, catalase activity, and superoxide dismutase activity. Post-treatment with CTXA resulted in a significant reduction in the deleterious renal functions by CLP, such as elevated BUN, creatinine, and urine protein. Induction of nitric oxide synthase and excessive production of nitric acid by CLP surgery were significantly reduced by post-treatment with CTXA via inhibiting nuclear factor-κB activation. Furthermore, the plasma levels of interleukin-6 and tumor necrosis factor-α were suppressed by CTXA post-treatment. Concurrently, CTXA treatment potently suppressed the CLP-induced septic lethality, rise of lipid peroxidation and markedly enhanced the antioxidant defense system by restoring the levels of superoxide dismutase, glutathione peroxidase, and catalase in kidney. The present results suggested that CTXA could protect against sepsis-triggered renal injury in mice.
[Mh] MeSH terms primary: Moraceae/chemistry
Plant Extracts/administration & dosage
Sepsis/drug therapy
Xanthones/administration & dosage
[Mh] MeSH terms secundary: Animals
Antioxidants/metabolism
Disease Models, Animal
Glutathione Peroxidase/genetics
Glutathione Peroxidase/metabolism
Humans
Interleukin-6/genetics
Interleukin-6/metabolism
Kidney/drug effects
Kidney/enzymology
Kidney/injuries
Male
Mice
NF-kappa B/genetics
NF-kappa B/metabolism
Sepsis/enzymology
Sepsis/genetics
Sepsis/metabolism
Superoxide Dismutase/genetics
Superoxide Dismutase/metabolism
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Antioxidants); 0 (Interleukin-6); 0 (NF-kappa B); 0 (Plant Extracts); 0 (Xanthones); 0 (cudratricusxanthone A); EC 1.11.1.9 (Glutathione Peroxidase); EC 1.15.1.1 (Superoxide Dismutase)
[Em] Entry month:1709
[Cu] Class update date: 170927
[Lr] Last revision date:170927
[Js] Journal subset:IM
[Da] Date of entry for processing:170610
[St] Status:MEDLINE

  7 / 2503 MEDLINE  
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[PMID]: 28536273
[Au] Autor:Aydemir TB; Kim MH; Kim J; Colon-Perez LM; Banan G; Mareci TH; Febo M; Cousins RJ
[Ad] Address:Food Science and Human Nutrition Department, Center for Nutritional Sciences, College of Agricultural and Life Sciences.
[Ti] Title:Metal Transporter ( ) Deletion in Mice Increases Manganese Deposition and Produces Neurotoxic Signatures and Diminished Motor Activity.
[So] Source:J Neurosci;37(25):5996-6006, 2017 Jun 21.
[Is] ISSN:1529-2401
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Mutations in human have been linked to symptoms of the early onset of Parkinsonism and Dystonia. This phenotype is likely related to excess manganese accumulation in the CNS. The metal transporter ZIP14 (SLC39A14) is viewed primarily as a zinc transporter that is inducible via proinflammatory stimuli. evidence shows that ZIP14 can also transport manganese. To examine a role for ZIP14 in manganese homeostasis, we used knock-out (KO) male and female mice to conduct comparative metabolic, imaging, and functional studies. Manganese accumulation was fourfold to fivefold higher in brains of KO mice compared with young adult wild-type mice. There was less accumulation of subcutaneously administered Mn in the liver, gallbladder, and gastrointestinal tract of the KO mice, suggesting that manganese elimination is impaired with ablation. Impaired elimination creates the opportunity for atypical manganese accumulation in tissues, including the brain. The intensity of MR images from brains of the KO mice is indicative of major manganese accumulation. In agreement with excessive manganese accumulation was the impaired motor function observed in the KO mice. These results also demonstrate that ZIP14 is not essential for manganese uptake by the brain. Nevertheless, the upregulation of signatures of brain injury observed in the KO mice demonstrates that normal ZIP14 function is an essential factor required to prevent manganese-linked neurodegeneration. Manganese is an essential micronutrient. When acquired in excess, manganese accumulates in tissues of the CNS and is associated with neurodegenerative disease, particularly Parkinson-like syndrome and dystonia. Some members of the ZIP metal transporter family transport manganese. Using mutant mice deficient in the ZIP14 metal transporter, we have discovered that ZIP14 is essential for manganese elimination via the gastrointestinal tract, and a lack of ZIP14 results in manganese accumulation in critical tissues such as the brain, as measured by MRI, and produces signatures of brain injury and impaired motor function. Humans with altered ZIP14 function would lack this gatekeeper function of ZIP14 and therefore would be prone to manganese-related neurological diseases.
[Mh] MeSH terms primary: Cation Transport Proteins/genetics
Cation Transport Proteins/metabolism
Manganese Poisoning/genetics
Manganese Poisoning/metabolism
Manganese/metabolism
Motor Activity/genetics
[Mh] MeSH terms secundary: Animals
Brain Chemistry/genetics
Female
Gastrointestinal Motility/genetics
Liver/metabolism
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Tissue Distribution
Zinc/metabolism
Zinc/pharmacology
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Cation Transport Proteins); 0 (SLC39A14 protein, mouse); 42Z2K6ZL8P (Manganese); J41CSQ7QDS (Zinc)
[Em] Entry month:1708
[Cu] Class update date: 170814
[Lr] Last revision date:170814
[Js] Journal subset:IM
[Da] Date of entry for processing:170525
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.0285-17.2017

  8 / 2503 MEDLINE  
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[PMID]: 28535124
[Au] Autor:Wijerathna TM; Gawarammana IB; Dissanayaka DM; Palanagasinghe C; Shihana F; Dassanayaka G; Shahmy S; Endre ZH; Mohamed F; Buckley NA
[Ad] Address:a South Asian Clinical Toxicology Research Collaboration, Faculty of Medicine , University of Peradeniya , Peradeniya , Sri Lanka.
[Ti] Title:Serum creatinine and cystatin C provide conflicting evidence of acute kidney injury following acute ingestion of potassium permanganate and oxalic acid.
[So] Source:Clin Toxicol (Phila);55(9):970-976, 2017 Nov.
[Is] ISSN:1556-9519
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:AIM: Acute kidney injury (AKI) is common following deliberate self-poisoning with a combination washing powder containing oxalic acid (H C O ) and potassium permanganate (KMnO ). Early and rapid increases in serum creatinine (sCr) follow severe poisoning. We investigated the relationship of these increases with direct nephrotoxicity in an ongoing multicenter prospective cohort study in Sri Lanka exploring AKI following poisoning. METHODS: Multiple measures of change in kidney function were evaluated in 48 consenting patients who had serial sCr and serum cystatin C (sCysC) data available. RESULTS: Thirty-eight (38/48, 79%) patients developed AKI (AKIN criteria). Twenty-eight (58%) had AKIN stage 2 or 3. Initial increases in urine creatinine (uCr) excretion were followed by a substantial loss of renal function. The AKIN stage 2 and 3 (AKIN2/3) group had very rapid rises in sCr (a median of 118% at 24 h and by 400% at 72 h post ingestion). We excluded the possibility that the rapid rise resulted from the assay used or muscle damage. In contrast, the average sCysC increase was 65% by 72 h. CONCLUSIONS: In most AKI, sCysC increases to the same extent but more rapidly than sCr, as sCysC has a shorter half-life. This suggests either a reduction in Cystatin C production or, conversely, that the rapid early rise of sCr results from increased production of creatine and creatinine to meet energy demands following severe oxidative stress mediated by H C O and KMnO . Increased early creatinine excretion supports the latter explanation, since creatinine excretion usually decreases transiently in AKIN2/3 from other causes.
[Mh] MeSH terms primary: Acute Kidney Injury/chemically induced
Creatinine/blood
Cystatin C/blood
Kidney/drug effects
Oxalic Acid/poisoning
Potassium Permanganate/poisoning
[Mh] MeSH terms secundary: Acute Kidney Injury/blood
Acute Kidney Injury/diagnosis
Acute Kidney Injury/physiopathology
Adult
Biomarkers/blood
Female
Glomerular Filtration Rate/drug effects
Humans
Kidney/metabolism
Kidney/physiopathology
Male
Muscle, Skeletal/drug effects
Muscle, Skeletal/metabolism
Muscle, Skeletal/pathology
Oxidative Stress/drug effects
Predictive Value of Tests
Prospective Studies
Reproducibility of Results
Severity of Illness Index
Sri Lanka
Suicide, Attempted
Time Factors
Young Adult
[Pt] Publication type:COMPARATIVE STUDY; JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Name of substance:0 (Biomarkers); 0 (CST3 protein, human); 0 (Cystatin C); 00OT1QX5U4 (Potassium Permanganate); 9E7R5L6H31 (Oxalic Acid); AYI8EX34EU (Creatinine)
[Em] Entry month:1709
[Cu] Class update date: 170911
[Lr] Last revision date:170911
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:170524
[St] Status:MEDLINE
[do] DOI:10.1080/15563650.2017.1326607

  9 / 2503 MEDLINE  
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[PMID]: 28504006
[Au] Autor:Zhang Y; Huang T; Xiao R; Xu H; Shen K; Zhou C
[Ad] Address:a Key Laboratory of Energy Thermal Conversion and Control of Ministry of Education, School of Energy and Environment , Southeast University , Nanjing , People's Republic of China.
[Ti] Title:A comparative study on the Mn/TiO -M(M = Sn, Zr or Al) O catalysts for NH -SCR reaction at low temperature.
[So] Source:Environ Technol;:1-11, 2017 May 29.
[Is] ISSN:0959-3330
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:A series of TiO -M(M = Sn, Zr or Al) O were prepared and manganese oxide (MnO ) was supported on the carrier by the traditional impregnation method for low-temperature selective catalytic reduction (SCR) of NO with ammonia as a reductant. The obtained catalysts were characterized by XRD, BET, high-resolution transmission electron microscope (HRTEM), H -TPR, NH -TPD, X-ray photoelectron spectroscopy (XPS) and in situ Fourier-transform infrared (FT-IR) and their catalytic activities for NO reduction with NH in the presence of SO were investigated comparatively. The results showed that the highest NO conversion of over 90% could be obtained with the Mn/Ti-Sn catalyst at a wide range of temperature window of 150-270°C. The combination of characterization techniques, such as BET, XRD and HRTEM, revealed that manganese oxides were well dispersed on Ti-Sn. H -TPR suggested that Ti-Sn and Ti-Zr supports could enhance the reduction ability of catalysts. Accordingly, Mn/Ti-Al exhibited worse activity at low temperature. XPS results were in good agreement with H -TPR results, and Mn/Ti-Sn had more surface-reducible species of Mn ions and more surface-adsorbed oxygen species, which was conducive to SCR reaction. The in situ FT-IR spectra of NH adsorption indicated that all the modified catalysts had more Lewis acid sites and the amide species at 1506 cm had a certain influence on the catalytic reaction at low temperature. Mn/Ti-Zr showed a stronger resistance to SO but Mn/Ti-Al was affected more adversely and all the catalysts could not be restored to the initial catalytic activity after stopping feeding SO . NH -TPD revealed that the total acid amount of the Mn/Ti-Sn sample was larger than other samples, which indicated that the Ti-Sn solid solution could provide more surface acid sites over the catalyst.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1705
[Cu] Class update date: 170622
[Lr] Last revision date:170622
[St] Status:Publisher
[do] DOI:10.1080/21622515.2017.1329345

  10 / 2503 MEDLINE  
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[PMID]: 28438148
[Au] Autor:Luo Y; McCullough LE; Tzeng JY; Darrah T; Vengosh A; Maguire RL; Maity A; Samuel-Hodge C; Murphy SK; Mendez MA; Hoyo C
[Ad] Address:Bioinformatics Research Center, North Carolina State University, Raleigh, NC, USA.
[Ti] Title:Maternal blood cadmium, lead and arsenic levels, nutrient combinations, and offspring birthweight.
[So] Source:BMC Public Health;17(1):354, 2017 Apr 24.
[Is] ISSN:1471-2458
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Cadmium (Cd), lead (Pb) and arsenic (As) are common environmental contaminants that have been associated with lower birthweight. Although some essential metals may mitigate exposure, data are inconsistent. This study sought to evaluate the relationship between toxic metals, nutrient combinations and birthweight among 275 mother-child pairs. METHODS: Non-essential metals, Cd, Pb, As, and essential metals, iron (Fe), zinc (Zn), selenium (Se), copper (Cu), calcium (Ca), magnesium (Mg), and manganese (Mn) were measured in maternal whole blood obtained during the first trimester using inductively coupled plasma mass spectrometry. Folate concentrations were measured by microbial assay. Birthweight was obtained from medical records. We used quantile regression to evaluate the association between toxic metals and nutrients due to their underlying wedge-shaped relationship. Ordinary linear regression was used to evaluate associations between birth weight and toxic metals. RESULTS: After multivariate adjustment, the negative association between Pb or Cd and a combination of Fe, Se, Ca and folate was robust, persistent and dose-dependent (p < 0.05). However, a combination of Zn, Cu, Mn and Mg was positively associated with Pb and Cd levels. While prenatal blood Cd and Pb were also associated with lower birthweight. Fe, Se, Ca and folate did not modify these associations. CONCLUSION: Small sample size and cross-sectional design notwithstanding, the robust and persistent negative associations between some, but not all, nutrient combinations with these ubiquitous environmental contaminants suggest that only some recommended nutrient combinations may mitigate toxic metal exposure in chronically exposed populations. Larger longitudinal studies are required to confirm these findings.
[Mh] MeSH terms primary: Birth Weight
Maternal Exposure/adverse effects
Metals, Heavy/blood
[Mh] MeSH terms secundary: Adult
Arsenic
Cadmium/blood
Copper/blood
Cross-Sectional Studies
Female
Folic Acid
Heavy Metal Poisoning
Humans
Iron/blood
Lead/blood
Manganese/blood
Poisoning
Selenium/blood
Socioeconomic Factors
Zinc/blood
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Metals, Heavy); 00BH33GNGH (Cadmium); 2P299V784P (Lead); 42Z2K6ZL8P (Manganese); 789U1901C5 (Copper); 935E97BOY8 (Folic Acid); E1UOL152H7 (Iron); H6241UJ22B (Selenium); J41CSQ7QDS (Zinc); N712M78A8G (Arsenic)
[Em] Entry month:1709
[Cu] Class update date: 171116
[Lr] Last revision date:171116
[Js] Journal subset:IM
[Da] Date of entry for processing:170426
[St] Status:MEDLINE
[do] DOI:10.1186/s12889-017-4225-8


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