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      Serum levels of trace minerals and heavy metals in severe COPD patients with and without pulmonary hypertension

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          Abstract

          Aim

          The aim of the current study was to assess the serum levels of trace minerals/heavy metals in COPD patients with and without pulmonary hypertension (PH) and to investigate their correlations to demographic, clinical, and biochemical variables.

          Materials and methods

          This cross-sectional study was performed in Van Yuzuncu Yil University Medical Faculty between April 2013 and July 2013. Cases were allocated into three groups: Group 1 consisted of severe COPD patients; Group 2 was made up of COPD patients with PH; and healthy controls constituted Group 3. Demographic, radiological, and biochemical variables, as well as the serum levels of trace minerals and heavy metals, were noted and compared in these three groups.

          Results

          COPD patients were older and had higher rates of smoking habit, diabetes mellitus, and hypertension compared to the control group. Carotid intima-media thickness was increased bilaterally, and serum levels of Co, Cu, and Fe were higher in COPD patients. Left carotid intima-media thickness was increased, and serum levels of Cd, Co, and Fe were found to be higher in COPD cases with PH compared to COPD patients without PH.

          Conclusion

          Our results show that serum levels of trace minerals and heavy metals may be altered in COPD and PH.

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          Most cited references 16

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          Trace elements in human physiology and pathology. Copper.

          Copper is a trace element, important for the function of many cellular enzymes. Copper ions can adopt distinct redox states oxidized Cu(II) or reduced (I), allowing the metal to play a pivotal role in cell physiology as a catalytic cofactor in the redox chemistry of enzymes, mitochondrial respiration, iron absorption, free radical scavenging and elastin cross-linking. If present in excess, free copper ions can cause damage to cellular components and a delicate balance between the uptake and efflux of copper ions determines the amount of cellular copper. In biological systems, copper homeostasis has been characterized at the molecular level. It is coordinated by several proteins such as glutathione, metallothionein, Cu-transporting P-type ATPases, Menkes and Wilson proteins and by cytoplasmic transport proteins called copper chaperones to ensure that it is delivered to specific subcellular compartments and thereby to copper-requiring proteins.
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            Elevated CO(2) levels cause mitochondrial dysfunction and impair cell proliferation.

            Elevated CO(2) concentrations (hypercapnia) occur in patients with severe lung diseases. Here, we provide evidence that high CO(2) levels decrease O(2) consumption and ATP production and impair cell proliferation independently of acidosis and hypoxia in fibroblasts (N12) and alveolar epithelial cells (A549). Cells exposed to elevated CO(2) died in galactose medium as well as when glucose-6-phosphate isomerase was knocked down, suggesting mitochondrial dysfunction. High CO(2) levels led to increased levels of microRNA-183 (miR-183), which in turn decreased expression of IDH2 (isocitrate dehydrogenase 2). The high CO(2)-induced decrease in cell proliferation was rescued by α-ketoglutarate and overexpression of IDH2, whereas proliferation decreased in normocapnic cells transfected with siRNA for IDH2. Also, overexpression of miR-183 decreased IDH2 (mRNA and protein) as well as cell proliferation under normocapnic conditions, whereas inhibition of miR-183 rescued the normal proliferation phenotype in cells exposed to elevated levels of CO(2). Accordingly, we provide evidence that high CO(2) induces miR-183, which down-regulates IDH2, thus impairing mitochondrial function and cell proliferation. These results are of relevance to patients with hypercapnia such as those with chronic obstructive pulmonary disease, asthma, cystic fibrosis, bronchopulmonary dysplasia, and muscular dystrophies.
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              Alterations of plasma magnesium, copper, zinc, iron and selenium concentrations and some related erythrocyte antioxidant enzyme activities in patients with Alzheimer's disease.

              The aim of the present study is to evaluate the status of plasma essential trace elements magnesium (Mg), copper (Cu), zinc (Zn), iron (Fe) and selenium (Se) concentrations and their some related antioxidant enzyme activities, erythrocyte glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT) activities in patients with Alzheimer's disease (AD). Fifty patients with AD and fifty healthy control subjects were included in this study. Plasma Cu and Zn concentrations by atomic absorption spectrometry (AAS), plasma Mg and Fe concentrations by spectrophotometric methods and plasma Se concentrations by graphite furnace AAS were determined. Erythrocyte GPx, SOD and CAT activities were measured by spectrophotometric methods. Plasma Mg, Cu, Zn, Fe and Se levels and erythrocyte GPx, SOD and CAT activities were found to be significantly lower in patients with AD compared with controls. These results suggest that alterations in essential trace elements and their related enzymes may play a role in the etiopathogenesis of AD. Also, there is a defect in the antioxidant defense system, which may lead to oxidative damage in patients with AD. The changes in antioxidant enzyme activities may be secondary to the alterations in their cofactor concentrations. Copyright 2010 Elsevier GmbH. All rights reserved.
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                Author and article information

                Journal
                Int J Chron Obstruct Pulmon Dis
                Int J Chron Obstruct Pulmon Dis
                International Journal of COPD
                International Journal of Chronic Obstructive Pulmonary Disease
                Dove Medical Press
                1176-9106
                1178-2005
                2018
                31 May 2018
                : 13
                : 1803-1808
                Affiliations
                [1 ]Department of Chest Diseases, Faculty of Medicine, Dursun Odabas Medical Center, Van Yuzuncu Yil University, Van, Turkey
                [2 ]Department of Cardiology, Medical Faculty, Van Yuzuncu Yil University, Van, Turkey
                [3 ]Department of Chemistry, Faculty of Science, Van Yuzuncu Yil University, Van, Turkey
                [4 ]Department of Internal Medicine, Faculty of Medicine, Van Yuzuncu Yil University, Van, Turkey
                [5 ]Department of Chest Diseases, Medical Faculty, Mugla University, Mugla, Turkey
                Author notes
                Correspondence: Selvi Asker, Department of Chest Diseases, Faculty of Medicine, Dursun Odabas Medical Center, Van Yuzuncu Yil University, Van 65100, Turkey, Tel +90 505 251 4704, Fax +90 432 212 1954, Email selviasker@ 123456yahoo.com
                Article
                copd-13-1803
                10.2147/COPD.S164431
                5987784
                © 2018 Asker et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

                Categories
                Original Research

                Respiratory medicine

                pulmonary hypertension, chronic obstructive pulmonary disease

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