Effects of hypoxia and reoxygenation on lung glutathione system

1990 ◽  
Vol 259 (2) ◽  
pp. H518-H524 ◽  
Author(s):  
R. M. Jackson ◽  
C. F. Veal
Keyword(s):  
Glutathione Peroxidase ◽  
Lung Tissue ◽  
Neutrophil Infiltration ◽  
Lavage Fluid ◽  
Glutathione System ◽  
Glutathione Disulfide ◽  
Lung Collapse ◽  
Total Glutathione ◽  
Reexpansion Pulmonary Edema ◽  
The Right

Reexpansion pulmonary edema (RPE) parallels reperfusion (reoxygenation) injuries in other organs in that hypoxic and hypoperfused lung tissue develops increased vascular permeability and neutrophil infiltration after reexpansion. This study investigated the lung cellular glutathione system during hypoxia (produced by lung collapse) and after reoxygenation (produced by reexpansion). Two separate groups of rabbits were studied to determine effects of lung hypoxia-reoxygenation on 1) lung glutathione peroxidase and reductase enzyme activities and 2) lung tissue, plasma, and alveolar lavage fluid total (reduced glutathione plus glutathione disulfide) and oxidized glutathione. Neither lung collapse for 3-7 days nor reexpansion for 2 h after 7 days of collapse affected glutathione peroxidase [controls, 0.36 +/- 0.04 (left), 0.38 +/- 0.03 U/mg DNA (right)] or reductase [controls, 0.12 +/- 0.01 (left), 0.14 +/- 0.01 U/mg DNA (right)] activities. The concentration of glutathione disulfide increased markedly in right alveolar lavage fluid, but not in plasma, after right lung reexpansion. Right lung total glutathione decreased significantly (-19%) after 7 days of collapse. After right lung reexpansion, both left (-65%) and right (-68%) lung total glutathione decreased significantly. The percent of total glutathione present in the oxidized form increased significantly in both left (to 15.5 +/- 4.0% of total) and right (to 18.7 +/- 6.3% of total) lungs after reexpansion of the right lung. These data indicate that lung tissue hypoxia, produced by unilateral lung collapse, was associated with a unilateral decrease in lung total glutathione content. Right lung reoxygenation, due to rapid reexpansion, caused a bilateral decrease in lung total glutathione content and an increase in right lung and alveolar lavage fluid glutathione disulfide concentration.

Glutathione levels and activities of glutathione metabolism enzymes in patients with schizophrenia: A systematic review and meta-analysis

2019 ◽  
Vol 33 (10) ◽  
pp. 1199-1214 ◽  
Author(s):  
Sakiko Tsugawa ◽  
Yoshihiro Noda ◽  
Ryosuke Tarumi ◽  
Yu Mimura ◽  
Kazunari Yoshida ◽  
...  
Keyword(s):  
Glutathione Peroxidase ◽  
Glutathione Reductase ◽  
Enzyme Activities ◽  
Glutathione Metabolism ◽  
First Episode ◽  
Glutathione Synthetase ◽  
Glutathione System ◽  
Glutathione Disulfide ◽  
Total Glutathione ◽  
Metabolism Enzymes

Background:Glutathione is among the important antioxidants to prevent oxidative stress. However, the relationships between abnormality in the glutathione system and pathophysiology of schizophrenia remain uncertain due to inconsistent findings on glutathione levels and/or glutathione-related enzyme activities in patients with schizophrenia.Methods:A systematic literature search was conducted using Embase, Medline, PsycINFO, and PubMed. Original studies, in which three metabolite levels (glutathione, glutathione disulfide, and total glutathione (glutathione+glutathione disulfide)) and five enzyme activities (glutathione peroxidase, glutathione reductase, glutamate-cysteine ligase, glutathione synthetase, and glutathione S-transferase) were measured with any techniques in both patients with schizophrenia and healthy controls, were included. Standardized mean differences were calculated to determine the group differences in the glutathione levels with a random-effects model.Results:We identified 41, 9, 15, 38, and seven studies which examined glutathione, glutathione disulfide, total glutathione, glutathione peroxidase, and glutathione reductase, respectively. Patients with schizophrenia had lower levels of both glutathione and total glutathione and decreased activity of glutathione peroxidase compared to controls. Glutathione levels were lower in unmedicated patients with schizophrenia than those in controls while glutathione levels did not differ between patients with first-episode psychosis and controls.Conclusions:Our findings suggested that there may be glutathione deficits and abnormalities in the glutathione redox cycle in patients with schizophrenia. However, given the small number of studies examined the entire glutathione system, further studies are needed to elucidate a better understanding of disrupted glutathione function in schizophrenia, which may pave the way for the development of novel therapeutic strategies in this disorder.

Endotoxin causes neutrophil-independent oxidative stress in rats

1988 ◽  
Vol 65 (1) ◽  
pp. 358-367 ◽  
Author(s):  
S. W. Chang ◽  
B. H. Lauterburg ◽  
N. F. Voelkel
Keyword(s):  
Oxidative Stress ◽  
Lung Injury ◽  
Lung Tissue ◽  
Salmonella Enteritidis ◽  
Reduced Glutathione ◽  
Platelet Activating Factor ◽  
Glutathione Disulfide ◽  
Total Glutathione ◽  
Arteriovenous Difference

Endotoxin-induced oxidative stress is investigated in rats by measuring changes in plasma and lung tissue levels of glutathione disulfide (GSSG) using a modified enzymatic assay that allows simultaneous measurement of up to 80 samples. Salmonella enteritidis endotoxin (2 and 20 mg/kg) acutely increased both plasma reduced glutathione and GSSG with a rise in the ratio of GSSG to total glutathione. This increase in GSSG was enhanced by pretreatment with 1,3-bis(2-chloroethyl)1-nitrosourea (BCNU), an inhibitor of the glutathione reductase enzyme. However, there was no significant arteriovenous difference in plasma GSSG across the lung, and lung tissue GSSG did not increase after endotoxin treatment. The increase in plasma GSSG was not blocked by vinblastine-induced neutropenia and could not be reproduced by incubating rat blood in vitro with endotoxin. Receptor antagonists of platelet-activating factor (PAF), at a dose that previously inhibited endotoxin-induced lung injury, attenuated the endotoxin-induced increase in plasma GSSG. We conclude that endotoxin causes neutrophil-independent oxidative stress in rats, which may be enhanced by the action of platelet-activating factor.

Endogenous and exogenous catalase in reoxygenation lung injury

1992 ◽  
Vol 72 (3) ◽  
pp. 858-864 ◽  
Author(s):  
R. M. Jackson ◽  
W. J. Russell ◽  
C. F. Veal
Keyword(s):  
Lung Injury ◽  
Pulmonary Edema ◽  
Catalase Activity ◽  
Neutrophil Infiltration ◽  
Progressive Increase ◽  
H2o2 Production ◽  
Lung Collapse ◽  
Extracellular Medium ◽  
Specific Effects ◽  
Reexpansion Pulmonary Edema

Reexpansion pulmonary edema parallels reperfusion (reoxygenation) injuries in other organs in that hypoxic and hypoperfused lung tissue develops increased vascular permeability and neutrophil infiltration after reexpansion. This study investigated endogenous lung catalase activity and H2O2 production during hypoxia (produced by lung collapse) and after reoxygenation (resulting from reexpansion), in addition to assessing the effects of exogenous catalase infusion on the development of unilateral pulmonary edema after reexpansion. Lung collapse resulted in a progressive increase in endogenous catalase activity after 3 (14%) and 7 days (23%), while activities in contralateral left lungs did not change (normal left lungs averaged 180 +/- 11 units/mg DNA). Tissue from control left lungs released H2O2 into the extracellular medium at a rate calculated to be 242 +/- 34 nmol.h-1.lung-1. No significant change in extracellular release of H2O2 occurred after 7 days of right lung collapse. However, after reexpansion of the previously collapsed right lungs for 2 h, H2O2 release from both reexpanded right and contralateral left lungs significantly increased (88 and 60%, respectively) compared with controls. Infusion of exogenous catalase significantly increased plasma and lung catalase activities. Exogenous catalase infusion prevented neither the increase in lung permeability nor the infiltration with neutrophils that typically occurs in reexpanded lungs. These data indicate that lung hypoxia/reoxygenation, induced by sequential collapse and reexpansion, has specific effects on endogenous lung catalase activity and H2O2 release. However, exogenous catalase does not prevent reexpansion pulmonary edema, eliminating extracellular (but not intracellular) H2O2 as an important mediator of unilateral lung injury in this model.

The “Spacemaker”, a New Device for Minimally Invasive Cardiothoracic Surgery: An Evaluation and Feasibility Study

2015 ◽  
Vol 10 (4) ◽  
pp. 241-247
Author(s):  
Pieter W.J. Lozekoot ◽  
Sandro Gelsomino ◽  
Paul B. Kwant ◽  
Orlando Parise ◽  
Francesco Matteucci ◽  
...  
Keyword(s):  
Minimally Invasive ◽  
Surgical Procedures ◽  
Lung Tissue ◽  
Lung Ventilation ◽  
Cardiothoracic Surgery ◽  
Respiratory Compromise ◽  
One Lung Ventilation ◽  
New Device ◽  
Lead Placement ◽  
The Right

Objective Our aim was to evaluate a new inflatable lung retractor, the “Spacemaker”, and its efficacy in facilitating minimally invasive cardiothoracic surgery without the need of one lung ventilation or carbon dioxide overpressure insufflation. Methods The device was tested in 12 anesthetized pigs (90–100 kg) placed on standard endotracheal ventilation. The device was introduced into the right or left side of the chest, depending on the intended procedure to be performed, via a 3-cm incision in the fifth intercostal space. A total of seven animals were used to evaluate hemodynamic and respiratory response to the device, whereas another five animals were used to assess the feasibility of a variety of minimally invasive cardiothoracic surgical procedures. Results Introduction was easy and unhindered. The device was inflated up to 0.6 bar, thereby pushing the lung tissue gently away cranially, posteriorly, and caudally without interfering with pulmonary function or resulting in respiratory compromise. In addition, hemodynamics remained stable throughout the experiments. Different closed-chest surgical procedures such as left atrial appendage exclusion, pulmonary vein exposure, pacemaker lead placement, and endoscopic stabilization for coronary surgery, were successfully performed. Removal was quick and complete in all cases, and lung tissue showed no remnant atelectasis. Conclusions The “Spacemaker” may represent a reliable alternative to current conventional techniques to facilitate minimally invasive cardiothoracic surgery. Further research is warranted to confirm the effectiveness and the safety of this device and to optimize the model before its use in humans and its introduction into clinical practice.

A new simple HPLC assay for the quantification of ertapenem in human plasma, lung tissue, and broncho-alveolar lavage fluid

2006 ◽  
Vol 832 (2) ◽  
pp. 231-235 ◽  
Author(s):  
R MUNDKOWSKI ◽  
J MAJCHERPESZYNSKA ◽  
O BURKHARDT ◽  
T WELTE ◽  
B DREWELOW
Keyword(s):  
Human Plasma ◽  
Lung Tissue ◽  
Lavage Fluid ◽  
Hplc Assay

scholarly journals Oxidative Stress in Rats After 60 Days of Hypergalactosemia or Hyperglycemia

2003 ◽  
Vol 22 (6) ◽  
pp. 423-427 ◽  
Author(s):  
Mary Otsyula ◽  
Matthew S. King ◽  
Tonya G. Ketcham ◽  
Ruth A. Sanders ◽  
John B. Watkins
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Insulin Treatment ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Glutathione Disulfide ◽  
Hepatic Lipid Peroxidation ◽  
Streptozotocin Diabetic Rats

Two of the models used in current diabetes research include the hypergalactosemic rat and the hyperglucosemic, streptozotocin-induced diabetic rat. Few studies, however, have examined the concurrence of these two models regarding the effects of elevated hexoses on biomarkers of oxidative stress. This study compared the activities of superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase and the concentrations of glutathione, glutathione disulfide, and thiobarbituric acid reactants (as a measure of lipid peroxidation) in liver, kidney, and heart of Sprague-Dawley rats after 60 days of either a 50% galactose diet or insulin deficiency caused by streptozotocin injection. Most rats from both models developed bilateral cataracts. Blood glucose and glycosy-lated hemoglobin A1c concentrations were elevated in streptozotocin diabetic rats. Streptozotocin diabetic rats exhibited elevated activities of renal superoxide dismutase, cardiac catalase, and renal and cardiac glutathione peroxidase, as well as elevated hepatic lipid peroxidation. Insulin treatment of streptozotocin-induced diabetic rats normalized altered markers. In galactosemic rats, hepatic lipid peroxidation was increased whereas glutathione reductase activity was diminished. Glutathione levels in liver were decreased in diabetic rats but elevated in the galactosemic rats, whereas hepatic glutathione disulfide concentrations were decreased much more in diabetes than in galactosemia. Insulin treatment reversed/prevented all changes caused by streptozotocin-induced diabetes. Lack of concomitance in these data indicate that the 60-day galactose-fed rat is not experiencing the same oxidative stress as the streptozotocin diabetic rat, and that investigators must be cautious drawing conclusions regarding the concurrence of the effects of the two animal models on oxidative stress biomarkers.

Class B Scavenger Receptors BI and BII Protect Against LPS-induced Acute Lung Injury in Mice by Mediating LPS Clearance

2021 ◽  
Author(s):  
Irina N. Baranova ◽  
Alexander V. Bocharov ◽  
Tatyana G. Vishnyakova ◽  
Zhigang Chen ◽  
Anna A. Birukova ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Transgenic Mice ◽  
Neutrophil Infiltration ◽  
Lavage Fluid ◽  
Protective Role ◽  
Lung Damage ◽  
Wild Type ◽  
Class B ◽  
Anti Inflammatory

Recent studies suggest an anti-inflammatory protective role for class B scavenger receptor BI (SR-BI) in endotoxin-induced inflammation and sepsis. Other data, including ours, provide evidence for an alternative role of SR-BI, facilitating bacterial and endotoxin uptake, and contributing to inflammation and bacterial infection. Enhanced endotoxin susceptibility of SR-BI deficient mice due to their anti-inflammatory glucocorticoid deficiency complicates understanding SR-BI’s role in endotoxemia/sepsis, calling for use of alternative models. In this study, using hSR-BI and hSR-BII transgenic mice, we found that SR-BI and to a lesser extent its splicing variant SR-BII, protects against LPS-induced lung damage. At 20 hours after intratracheal LPS instillation the extent of pulmonary inflammation and vascular leakage was significantly lower in hSR-BI and hSR-BII transgenic mice compared to wild type mice. Higher bronchoalveolar lavage fluid (BALF) inflammatory cell count and protein content as well as lung tissue neutrophil infiltration found in wild type mice was associated with markedly (2-3 times) increased pro-inflammatory cytokine production as compared to transgenic mice following LPS administration. Markedly lower endotoxin levels detected in BALF of transgenic vs. wild type mice along with the significantly increased BODIPY-LPS uptake observed in lungs of hSR-BI and hSR-BII mice 20 hours after the IT LPS injection suggest that hSR-BI and hSR-BII-mediated enhanced LPS clearance in the airways could represent the mechanism of their protective role against LPS-induced acute lung injury.

scholarly journals Mechanical Ventilation Enhances Acinetobacter Baumannii-induced Lung Injury Through JNK Pathways

2021 ◽  
Author(s):  
Tzyy-Bin Tsay ◽  
Wan-Hsuan Chang ◽  
Ching-Mei Hsu ◽  
Lee-Wei Chen
Keyword(s):  
Mechanical Ventilation ◽  
Lung Injury ◽  
Acinetobacter Baumannii ◽  
Neutrophil Infiltration ◽  
Lavage Fluid ◽  
Protein Levels ◽  
Killing Activity ◽  
Nitrite Production ◽  
Bacteria Killing ◽  
Factor Α

Abstract Background: Patients in intensive care units (ICUs) often received broad-spectrum antibiotic treatment and Acinetobacter baumannii (A.b.) and Pseudomonas aeruginosa (P.a.) were the most common pathogens causing ventilator-associated pneumonia (VAP). This study aimed to examine the effects and mechanism of mechanical ventilation (MV) on A.b.-induced lung injury and the involvement of alveolar macrophages (AMs).Methods: C57BL/6 wild-type (WT) and c-Jun N-terminal kinase knockout (JNK1−/−) mice received MV for 3 h at 2 days after nasal instillation of A.b., P.a. (1 × 106 colony-forming unit, CFU), or normal saline.Results: Intranasal instillation of 106 CFU A.b. in C57BL/6 mice induced a significant increase in total cells and protein levels in the bronchoalveolar lavage fluid (BALF) and neutrophil infiltration in the lungs. MV after A.b. instillation increases neutrophil infiltration, interleukin (IL)-6 and vascular cell adhesion molecule (VCAM) mRNA expression in the lungs and total cells, IL-6 levels, and nitrite levels in the BALF. The killing activity of AMs against A.b. was lower than against P.a. The diminished killing activity was parallel with decreased tumor necrosis factor-α production by AMs compared with with A.b. Moreover, MV decreased the A.b. and P.a. killing activity of AMs. MV after A.b. instillation induced less total cells in the BALF and nitrite production in the serum of JNK1-/- mice than those of WT mice.Conclusion: A.b. is potent in inducing neutrophil infiltration in the lungs and total protein in the BALF. MV enhances A.b.-induced lung injury through an increase in the expression of VCAM and IL-6 levels in the BALF and a decrease in the bacteria-killing activity of AMs. A lower inflammation level in JNK1-/- mice indicates that A.b.-induced VAP causes lung injury through JNK signaling pathway in the lungs.

scholarly journals Human neutrophil lipocalin (HNL) and myeloperoxidase (MPO). Studies of lung lavage fluid and lung tissue

2000 ◽  
Vol 94 (6) ◽  
pp. 564-568 ◽  
Author(s):  
B. SCHMEKEL ◽  
L. SEVEUS ◽  
S.Y. XU ◽  
P. VENGE
Keyword(s):  
Lung Tissue ◽  
Human Neutrophil ◽  
Lavage Fluid ◽  
Lung Lavage

Carcinoma of the Right Bronchus

1929 ◽  
Vol 44 (12) ◽  
pp. 830-832 ◽  
Author(s):  
Thacker Neville
Keyword(s):  
Lung Tissue ◽  
Great Majority ◽  
Primary Carcinoma ◽  
Malignant Tumours ◽  
The Right

Malignant tumours of the bronchus were not recognised till comparatively recently. Adler, in 1912, is said to have been the first to report such a tumour. The great majority of new growths of the lung originate in the bronchi and subsequently invade the lung tissue. Primary carcinoma of the lung is not as rare as it used to be, for formerly it was said to occur in less than 1 per cent, of all primary carcinomas; but statistics from Hamburg and Leipzig reveal at times an incidence as high as 9-4 per cent, to 15-5 per cent., whilst Vinson, Moersch, and Kirklin have diagnosed Tj cases of primary carcinoma of the lung between 1925 and 1928, and Macrae, Funk and Jackson observed 13 cases and mentioned 128 cases reported by other authors.

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