scholarly journals Alterations of Erythrocyte Superoxide Dismutase activity in patients suffering from asthma attacks

2016 ◽  
Vol 73 (3) ◽  
Author(s):  
K. Katsoulis ◽  
T. Kontakiotis ◽  
S. Gerou ◽  
M. Kougioulis ◽  
H. Lithoxopoulou ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Defense Mechanism ◽  
Colorimetric Method ◽  
Forced Expiratory Volume ◽  
Arterial Oxygen ◽  
Severe Exacerbation ◽  
Sod Activity ◽  
Asthmatic Patients ◽  
Asthma Attack ◽  
Erythrocyte Superoxide Dismutase

Background. Oxidant-antioxidant imbalance may play an important role in the development and progression of bronchial asthma. However, the role of blood antioxidants especially in asthma exacerbation has not been fully discussed. Objective. This study examines a part of the intracellular antioxidant defense mechanism in asthmatic patients admitted to hospital due to severe exacerbation of their disease. Methods. Peripheral blood Erythrocyte Superoxide Dismutase (SOD) activity was measured in 38 patients (33 men - 5 women, with a mean age of 56±2.8 yrs), using a colorimetric method. On the days of admission and discharge the Forced Expiratory Volume in 1 second (FEV1) and the Partial arterial Oxygen pressure (PaO2) were recorded and correlated with SOD activity at the same time. Results. A statistically significant decrease of SOD activity was observed on the day of admission compared to SOD activity on the day of discharge (43.64±31.78 vs. 96.16±54.05 units/ml, p<0.001), suggesting the presence of oxidative stress during an asthma attack. A statistically significant correlation was observed between FEV1 on admission and SOD activity at the same time (r=0.57, p<0.001). Furthermore, SOD activity on admission was correlated with PaO2 on discharge (r=0.55, p<0.001), as well as SOD on discharge with PaO2 on discharge (r=0.53, p=0.001). Conclusions. Decreased systemic erythrocyte SOD activity was observed during asthma attacks. This activity was correlated with severity criteria such as FEV1 and PaO2. Therefore, it seems that measurement of SOD activity could be a useful tool in the evaluation of an asthma attack. The supplementary administration of antioxidants in the future needs further clarification.

scholarly journals Enhancement of erythrocyte superoxide dismutase activity: effects on cellular oxidant defense

Blood ◽  
1989 ◽  
Vol 74 (7) ◽  
pp. 2542-2549 ◽  
Author(s):  
MD Scott ◽  
JW Eaton ◽  
FA Kuypers ◽  
DT Chiu ◽  
BH Lubin
Keyword(s):  
Superoxide Dismutase ◽  
Hemoglobin Concentration ◽  
Thiobarbituric Acid ◽  
Sod Activity ◽  
Control Value ◽  
Menadione Sodium Bisulfite ◽  
Erythrocyte Superoxide Dismutase ◽  
Additional Protection ◽  
Normal Human ◽  
Cellular Deformability

To delineate further the role of superoxide dismutase (SOD) in red blood cell (RBC) oxidant defense, normal human erythrocytes were osmotically lysed and resealed in the presence of varying concentrations of exogenous SOD. This resulted in a dose-dependent increase in SOD activity in the resealed erythrocytes while maintaining nearly normal RBC hemoglobin concentration (less than 10% decrease from the control value), cell volume, and cellular deformability. Surprisingly, a five- or ninefold increase in SOD activity yielded no additional protection against superoxide-generating drugs (phenazine methosulfate or menadione sodium bisulfite). No significant differences were observed between the control and SOD-loaded RBCs in O2-driven methemoglobin formation or generation of thiobarbituric acid-reactive substances. In contrast, RBCs with elevated SOD activity pretreated with sodium azide (to block catalase activity) or 1-chloro-2,4- dinitrobenzene (to deplete reduced glutathione, GSH) showed significantly enhanced methemoglobin generation in response to superoxide generating drugs. No differential response was noted between the control, control-resealed, and SOD-loaded RBCs to oxidants other than superoxide. Based on our results and other data, we conclude that elevated SOD activity may imbalance cellular oxidant defense, resulting in enhanced oxidation due to the accelerated generation of H2O2, the product of O2- dismutation. This effect is significantly exacerbated under conditions in which H2O2 catabolism is altered.

scholarly journals Enhancement of erythrocyte superoxide dismutase activity: effects on cellular oxidant defense

Blood ◽  
1989 ◽  
Vol 74 (7) ◽  
pp. 2542-2549 ◽  
Author(s):  
MD Scott ◽  
JW Eaton ◽  
FA Kuypers ◽  
DT Chiu ◽  
BH Lubin
Keyword(s):  
Superoxide Dismutase ◽  
Hemoglobin Concentration ◽  
Thiobarbituric Acid ◽  
Sod Activity ◽  
Control Value ◽  
Menadione Sodium Bisulfite ◽  
Erythrocyte Superoxide Dismutase ◽  
Additional Protection ◽  
Normal Human ◽  
Cellular Deformability

Abstract To delineate further the role of superoxide dismutase (SOD) in red blood cell (RBC) oxidant defense, normal human erythrocytes were osmotically lysed and resealed in the presence of varying concentrations of exogenous SOD. This resulted in a dose-dependent increase in SOD activity in the resealed erythrocytes while maintaining nearly normal RBC hemoglobin concentration (less than 10% decrease from the control value), cell volume, and cellular deformability. Surprisingly, a five- or ninefold increase in SOD activity yielded no additional protection against superoxide-generating drugs (phenazine methosulfate or menadione sodium bisulfite). No significant differences were observed between the control and SOD-loaded RBCs in O2-driven methemoglobin formation or generation of thiobarbituric acid-reactive substances. In contrast, RBCs with elevated SOD activity pretreated with sodium azide (to block catalase activity) or 1-chloro-2,4- dinitrobenzene (to deplete reduced glutathione, GSH) showed significantly enhanced methemoglobin generation in response to superoxide generating drugs. No differential response was noted between the control, control-resealed, and SOD-loaded RBCs to oxidants other than superoxide. Based on our results and other data, we conclude that elevated SOD activity may imbalance cellular oxidant defense, resulting in enhanced oxidation due to the accelerated generation of H2O2, the product of O2- dismutation. This effect is significantly exacerbated under conditions in which H2O2 catabolism is altered.

Erythrocyte superoxide dismutase deficiency in Fanconi's anaemia established by two independent methods of assay

1979 ◽  
Vol 39 (8) ◽  
pp. 759-764 ◽  
Author(s):  
H. Joenje ◽  
R. R. Frants ◽  
F. Arwert ◽  
G. J. M. De Bruin ◽  
P. J. Kostense ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Erythrocyte Superoxide Dismutase

scholarly journals Air Trapping Is Associated with Heterozygosity for Alpha-1 Antitrypsin Mutations in Patients with Asthma

Respiration ◽  
2021 ◽  
pp. 1-10
Author(s):  
Marina Aiello ◽  
Marianna Ghirardini ◽  
Laura Marchi ◽  
Annalisa Frizzelli ◽  
Roberta Pisi ◽  
...  
Keyword(s):  
Lung Function ◽  
Serum Concentration ◽  
Forced Expiratory Volume ◽  
Small Airway ◽  
University Hospital ◽  
Air Trapping ◽  
Asthmatic Patients ◽  
Alpha 1 Antitrypsin Deficiency ◽  
Alpha 1 Antitrypsin ◽  
Few Data

<b><i>Background:</i></b> Alpha-1 antitrypsin deficiency (AATD) is a hereditary disorder involving lungs, characterized by low serum concentration of the protein alpha-1 antitrypsin (AAT) also called proteinase inhibitor (PI). Asthma is common in AATD patients, but there are only few data on respiratory function in asthmatic patients with AATD. <b><i>Objectives:</i></b> The aim of the study was to evaluate lung function in asthmatic outpatients with mutation in the <i>SERPINA1</i> gene coding for AAT versus asthmatic subjects without mutation. <b><i>Methods:</i></b> We performed the quantitative analysis of the serum concentration of AAT in 600 outpatients affected by mild to moderate asthma from the University Hospital of Parma, Italy. Fifty-seven of them underwent the genetic analysis subsequently; they were subdivided into mutated and non-mutated subjects. All the mutated patients had a heterozygous genotype, except 1 (PI*SS). We assessed the lung function through a flow-sensing spirometer and the small airway parameters through an impulse oscillometry system. <b><i>Results:</i></b> The values of forced vital capacity (% predicted) and those of the residual volume to total lung capacity ratio (%) were, respectively, lower and higher in patients mutated versus patients without mutation, showing a significantly greater air trapping (<i>p =</i> 0.014 and <i>p =</i> 0.017, respectively). Moreover, patients with mutation in comparison to patients without mutation showed lower forced expiratory volume in 3 s (% predicted) and forced expiratory volume in 6 s (L) spirometric values, reflecting a smaller airways contribution. <b><i>Conclusions:</i></b> In asthmatic patients, heterozygosity for AAT with PI*MZ and PI*MS genotypes was associated with small airway dysfunction and with lung air trapping.

10-gingerol induces oxidative stress through HTR1A in cumulus cells: in-vitro and in-silico studies

2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Kiptiyah Kiptiyah ◽  
Widodo Widodo ◽  
Gatot Ciptadi ◽  
Aulanni’am Aulanni’Am ◽  
Mohammad A. Widodo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Culture ◽  
Superoxide Dismutase ◽  
In Silico ◽  
Cumulus Cell ◽  
Cumulus Cells ◽  
Sod Activity ◽  
In Silico Studies ◽  
Incubation Periods

AbstractBackgroundWe investigated whether 10-gingerol is able to induce oxidative stress in cumulus cells.MethodsFor the in-vitro research, we used a cumulus cell culture in M199, containing 10-gingerol in various concentrations (0, 12, 16, and 20 µM), and detected oxidative stress through superoxide dismutase (SOD) activity and malondialdehyde (MDA) concentrations, with incubation periods of 24, 48, 72, and 96 h. The obtained results were confirmed by in-silico studies.ResultsThe in-vitro data revealed that SOD activity and MDA concentration increased with increasing incubation periods: SOD activity at 0 µM (1.39 ± 0.24i), 12 µM (16.42 ± 0.35ab), 16 µM (17.28 ± 0.55ab), 20 µM (17.81 ± 0.12a), with a contribution of 71.1%. MDA concentration at 0 µM (17.82 ± 1.39 l), 12 µM (72.99 ± 0.31c), 16 µM (79.77 ± 4.19b), 20 µM (85.07 ± 2.57a), with a contribution of 73.1%. Based on this, the in-silico data uncovered that 10˗gingerol induces oxidative stress in cumulus cells by inhibiting HTR1A functions and inactivating GSK3B and AKT˗1.Conclusions10-gingerol induces oxidative stress in cumulus cells through enhancing SOD activity and MDA concentration by inhibiting HTR1A functions and inactivating GSK3B and AKT˗1.

scholarly journals Bovine Erythrocyte Superoxide Dismutase

1974 ◽  
Vol 249 (22) ◽  
pp. 7339-7347
Author(s):  
John L. Abernethy ◽  
Howard M. Steinman ◽  
Robert L. Hill
Keyword(s):  
Superoxide Dismutase ◽  
Bovine Erythrocyte ◽  
Erythrocyte Superoxide Dismutase

scholarly journals Attenuation of renal excretory responses to ANG II during inhibition of superoxide dismutase in anesthetized rats

2010 ◽  
Vol 298 (2) ◽  
pp. F401-F407 ◽  
Author(s):  
Md. Abdul Hye Khan ◽  
Mohammed Toriqul Islam ◽  
Alexander Castillo ◽  
Dewan Syed Abdul Majid
Keyword(s):  
Superoxide Dismutase ◽  
Nadph Oxidase ◽  
Oxidase Activity ◽  
Ang Ii ◽  
Sod Activity ◽  
Doppler Flowmetry ◽  
Nadph Oxidase Activity ◽  
Blood Flows ◽  
Renal Responses

To examine the functional interaction between superoxide dismutase (SOD) and NADPH oxidase activity, we assessed renal responses to acute intra-arterial infusion of ANG II (0.5 ng·kg−1·min−1) before and during administration of a SOD inhibitor, diethyldithiocarbamate (DETC, 0.5 mg·kg−1·min−1), in enalaprilat-pretreated (33 μg·kg−1·min−1) rats ( n = 11). Total (RBF) and regional (cortical, CBF; medullary; MBF) renal blood flows were determined by Transonic and laser-Doppler flowmetry, respectively. Renal cortical and medullary tissue NADPH oxidase activity in vitro was determined using the lucigenin-chemiluminescence method. DETC treatment alone resulted in decreases in RBF, CBF, MBF, glomerular filtration rate (GFR), urine flow (V), and sodium excretion (UNaV) as reported previously. Before DETC, ANG II infusion decreased RBF (−18 ± 3%), CBF (−16 ± 3%), MBF [−5 ± 6%; P = not significant (NS)], GFR (−31 ± 4%), V (−34 ± 2%), and UNaV (−53 ± 3%). During DETC infusion, ANG II also caused similar reductions in RBF (−20 ± 4%), CBF (−19 ± 3%), MBF (−2 ± 2; P = NS), and in GFR (−22 ± 7%), whereas renal excretory responses (V; −12 ± 2%; UNaV; −24 ± 4%) were significantly attenuated compared with those before DETC. In in vitro experiments, ANG II (100 μM) enhanced NADPH oxidase activity both in cortical [13,194 ± 1,651 vs. 20,914 ± 2,769 relative light units (RLU)/mg protein] and in medullary (21,296 ± 2,244 vs. 30,597 ± 4,250 RLU/mg protein) tissue. Application of DETC (1 mM) reduced the basal levels and prevented ANG II-induced increases in NADPH oxidase activity in both tissues. These results demonstrate that renal excretory responses to acute ANG II administration are attenuated during SOD inhibition, which seems related to a downregulation of NADPH oxidase in the deficient condition of SOD activity.

Anxiety in Asthma: Panic-Fear Symptomatology and Personality in Relation to Manifest Anxiety

1980 ◽  
Vol 46 (1) ◽  
pp. 196-198 ◽  
Author(s):  
Robert A. Kinsman ◽  
Jerald F. Dirks ◽  
Nancy Wray Dahlem ◽  
Audrey S. Heller
Keyword(s):  
Trait Anxiety ◽  
State Anxiety ◽  
Symptom Scale ◽  
Asthmatic Patients ◽  
Asthma Attack ◽  
Taylor Manifest Anxiety Scale ◽  
Symptom Reports ◽  
Symptom Scores ◽  
Manifest Anxiety ◽  
Moderate Relationship

Anxiety in asthma has been measured in two ways. The MMPI Panic-Fear scale is a measure of general, nonillness specific anxiety and the Panic-Fear symptom scale of the Asthma Symptom Checklist is a measure of illness-specific anxiety focused on the asthma attack. Both measures relate to response styles in asthma which contribute to the maintenance of illness. In the present study of 140 asthmatic patients, MMPI Panic-Fear scores were highly related to trait-anxiety measured by the Taylor Manifest Anxiety Scale, even after partialling out checklist Panic-Fear symptom scores. In contrast, Panic-Fear symptomatology had a more moderate relationship to the Taylor Anxiety scores and was independent of the Taylor scores after partialling out MMPI Panic-Fear scores. The results support earlier findings suggesting that MMPI Panic-Fear measures trait anxiety. In contrast, checklist Panic-Fear symptom reports measure an illness-specific state anxiety that is not per se a measure of trait anxiety.

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