Thiol Levels in Rat Bronchio-Alveolar Lavage Fluid after Administration of Cysteine Esters

1994 ◽  
Vol 13 (11) ◽  
pp. 776-780 ◽  
Author(s):  
Alison F. Lailey ◽  
David G. Upshall
Keyword(s):  
Pulmonary Oedema ◽  
Plasma Levels ◽  
Dimethyl Ester ◽  
Intraperitoneal Administration ◽  
Pyrolysis Product ◽  
Lavage Fluid ◽  
Lethal Effects ◽  
Tertiary Butyl ◽  
Butyl Esters ◽  
Close Proximity

1 The intraperitoneal administration of cysteine, N-acetylcysteine, the methyl, isopropyl, cyclo pentyl, neo pentyl, cyclo hexyl and tertiary butyl esters of cysteine and of cystine dimethyl ester increased the levels of total non-protein sulphydryls and cysteine in the bronchioalveolar lavage fluid and plasma of rats. In all cases the non-protein sulphydryl levels reflected the increased cysteine levels. 2 Cysteine, N-acetylcysteine, the cysteine esters and cystine dimethyl ester raised the levels of non-protein sulphydryls and hence cysteine in the bronchioalveolar lining fluid as follows: CIPE > CCPE > CME > CDME > CneoPE > CCHE > Nac > CySH > CTBE. 3 Plasma levels of NPSH were increased as follows: Nac > CySH > CCPE > CCHE > CneoPE > CIPE > CME > CDME > CTBE. 4 All except CTBE have been shown to protect against the lethal effects of inhaled perfluoroisobutene, a pyrolysis product of polytetrafluoroethene which induces a fulminating pulmonary oedema. 5 This study showed that by raising the levels of thiols in the bronchioalveolar lavage fluid (BALF), the epithelial cells lining the bronchiolar, alveolar regions of the lung could be protected against inhaled toxicants. 6 It is proposed that increased thiol levels in the BALF may contribute to the overall protection induced by these compounds by reacting with inhaled electrophiles to prevent or reduce damage to tissue in close proximity to the airways.

Oral N-acetylcysteine protects against perfluoroisobutene toxicity in rats

1997 ◽  
Vol 16 (4) ◽  
pp. 212-216 ◽  
Author(s):  
Alison F Lailey
Keyword(s):  
Oral Administration ◽  
Pulmonary Oedema ◽  
Plasma Levels ◽  
Pyrolysis Product ◽  
Lavage Fluid ◽  
Lethal Effects ◽  
Duration Of Protection ◽  
Gas Exposure

1 Perfluoroisobutene, a pyrolysis product of polytetra fluoroethene may cause pulmonary oedema and death when inhaled. Oral N-acetylcysteine has shown protection against inhalation of perfluoroisobutene and in this study we have tried to elucidate the mechanism by which protection is mediated. 2 Protection against the lethal effects of inhaled per fluoroisobutene has been shown when N-acetylcys teine has been orally administered 4, 6 or 8 h before gas exposure. 3 Plasma levels of cysteine, glutathione and N-acetylcys teine were increased for up to 7 h following oral administration of Nac. 4 N-acetylcysteine was not detected in the bronchio alveolar lavage fluid following oral administration. 5 Duration of protection in vivo has been related to the duration of increased thiol levels in the plasma.

Titration syntheses of polyaminosubstituted phthalocyanines via nucleophilic aromatic substitutions on zinc(II) 1,2,3,4,8,9,10,11,15,16,17,18,22,23,24,25-hexadecafluorophthalocyanine

2007 ◽  
Vol 11 (07) ◽  
pp. 537-546 ◽  
Author(s):  
Clifford C. Leznoff ◽  
Annette Hiebert ◽  
Sibel Ok
Keyword(s):  
Amino Acids ◽  
Chain Length ◽  
Secondary Amines ◽  
Primary Amines ◽  
Tertiary Butyl ◽  
Butyl Esters ◽  
Mild Conditions ◽  
Nucleophilic Aromatic Substitutions

Primary amines, secondary amines and tertiary butyl esters of amino acids are used as nucleophiles with zinc(II) hexadecafluorophthalocyanine to provide mixtures of mono and disubstituted fluorinated phthalocyanines under mild conditions, or polyaminosubstituted phthalocyanines when using the amines as solvents. Diamines give cyclic substituted phthalocyanines, binuclear or trinuclear phthalocyanines or mixtures of both types, depending on the chain length or structure of the diamine.

scholarly journals Radon as a Natural Tracer for Monitoring NAPL Groundwater Contamination

Water ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 3327
Author(s):  
Martina Mattia ◽  
Paola Tuccimei ◽  
Michele Soligo ◽  
Claudio Carusi
Keyword(s):  
Noble Gas ◽  
Water Soluble ◽  
Source Zone ◽  
Contaminated Site ◽  
Butyl Ether ◽  
Good Correspondence ◽  
Tertiary Butyl ◽  
Local Reduction ◽  
Close Proximity ◽  
Natural Tracer

In this research, the radioactive noble gas radon was used as a tracer for Non-Aqueous Phase Liquids (NAPLs) contamination, since it is much more soluble in these substances than in air or water. Soil radon remains trapped within the NAPLs, resulting in a local reduction in the radon concentration within close proximity to the contaminated area. This technique was applied to a contaminated site in Roma (Italy). The main residual NAPLs are total hydrocarbons and methyl-tertiary-butyl ether (MTBE), a water-soluble additive. The monitoring activities included two sampling campaigns of groundwater from 18 wells in February and May 2020. Concentration maps were produced using radon data. The results show that the radon deficit traces the location of NAPLs in the fuelling station very well, with a residual source zone extending in a NNW-SSE direction. A good correspondence between a low amount of radon and a higher concentration of NAPLs was found. A reduction in the average amount of radon in the May 2020 survey indicated a stronger remobilization of NAPLs compared to that of the February 2020 monitoring campaign. The peaks of Volatile Organic Compounds (VOCs) detected between 8–9 and 11–12 m depths indicate the presence of residual blobs of NAPLs in the vadose zone of the aquifer.

The effect of perfluoroisobutene and phosgene on rat lavage fluid surfactant phospholipids

1999 ◽  
Vol 18 (11) ◽  
pp. 659-668 ◽  
Author(s):  
B Jugg ◽  
J Jenner ◽  
P Rice
Keyword(s):  
Pulmonary Oedema ◽  
High Performance ◽  
Solid Phase ◽  
Inflammatory Cells ◽  
Lavage Fluid ◽  
Rat Lung ◽  
Air Exposure ◽  
Surfactant System ◽  
Type Ii Pneumocytes ◽  
Surfactant Phospholipids

1 This study investigated whether the reactive organohalogen gases perfluoroisobutene (PFIB) and phosgene, which cause death by overwhelming pulmonary oedema, affect the surfactant system or type II pneumocytes of rat lung. 2 The progression and type of pulmonary injury in Porton Wistar-derived rats was monitored over a 48 h period following exposure to either PFIB or phosgene (LCt30) by analyzing the inflammatory cells and protein in bronchoalveolar lavage fluid. Six rat lung phospholipids were measured by high-performance liquid chromatography, following solid phase extraction from lavage fluid. 3 Alterations in the cell population and lung permeability occurred following both gases, indicating that the injury was a permeability-type pulmonary oedema. Changes in the total amount of phospholipid and in the percentage composition of the surfactant were different for the two gases. PFIB produced increases in phosphatidylglycerol and phosphatidylcholine over the first hour, similar to that seen following air exposure, followed by substantial decreases in these phospholipids. Phosgene caused late increases in all phospholipids from 6 h post-exposure. 4 Differences in the response of the surfactant system to exposure to PFIB and phosgene suggest different mechanisms of action at the alveolar surface although the final injurious response is pulmonary oedema for both gases.

scholarly journals Protection from experimental ventilator-induced acute lung injury by IL-1 receptor blockade

Thorax ◽  
2007 ◽  
Author(s):  
James A Frank ◽  
Jean-Francois Pittet ◽  
Charlie Wray ◽  
Michael A. Matthay
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Plasma Levels ◽  
Injury Severity ◽  
Cell Injury ◽  
Lavage Fluid ◽  
Early Event ◽  
Type I ◽  
Barrier Dysfunction ◽  
Type Ii Pneumocytes

Background: Clinical studies have shown that injurious mechanical ventilation is associated with elevated airspace and plasma levels of interleukin-1β (IL-1β); however, the potential therapeutic value of IL-1 inhibition in acute lung injury has not been thoroughly investigated. A study was undertaken to determine if IL-1 signaling is a necessary early event in the pathogenesis of experimental ventilator-induced lung injury (VILI). Methods: Mice deficient in IL-1 receptor type 1 (IL1R1) and rats treated with IL-1 receptor antagonist (IL-1Ra) were mechanically ventilated with high tidal volume (30 ml/kg) and the effect of IL-1 signaling blockade on lung injury severity was determined. Results: Permeability as measured by radiolabeled albumin flux was significantly lower in IL1R1 null mice compared with wild type mice during injurious ventilation (P<0.05). IL-1Ra significantly decreased protein permeability and pulmonary oedema in rats during injurious ventilation. IL-1Ra also decreased airspace and plasma levels of the chemokine CXCL1 and airspace neutrophils. IL-1Ra decreased expression of NOS2 and ICAM-1 mRNA in whole lung. Bronchoalveolar lavage fluid levels of RTI40, a marker of type I cell injury, were 2.5 times lower in following IL-1Ra treatment (P < 0.05). In isolated type II pneumocytes, IL-1β reduced electrical resistance and increased transepithelial permeability. Conclusions: IL-1 contributes to alveolar barrier dysfunction in VILI by promoting lung neutrophil recruitment, and by increasing epithelial injury and permeability. Because preserved alveolar barrier function is associated with better outcomes in patients with acute lung injury, these data support further testing of IL-1Ra for the treatment of acute lung injury.

Reduction of allergic airway eosinophilia by dietary raffinose in Brown Norway rats

2004 ◽  
Vol 92 (2) ◽  
pp. 247-255 ◽  
Author(s):  
Hiroshi Watanabe ◽  
Kei Sonoyama ◽  
Jun Watanabe ◽  
Natsu Yamaguchi ◽  
Hiroto Kikuchi ◽  
...  
Keyword(s):  
Human Subjects ◽  
Control Diet ◽  
Disease Model ◽  
Intraperitoneal Administration ◽  
Lavage Fluid ◽  
Brown Norway ◽  
Intragastric Administration ◽  
Mrna Levels ◽  
Airway Eosinophilia ◽  
Norway Rats

Oral administration of raffinose, a naturally occurring indigestible oligosaccharide, has reportedly ameliorated atopic dermatitis in human subjects although the mechanism is unknown. The present study investigated the effect of dietary raffinose on allergen-induced airway eosinophilia in ovalbumin-sensitised Brown Norway rats as an atopic disease model. Brown Norway rats were immunised by subcutaneous injection with ovalbumin on day 0 and fed either a control diet or the diet supplemented with raffinose (50 g/kg diet). The rats were exposed to aerosolised ovalbumin on day 20, and broncho-alveolar lavage fluid was obtained on the next day. The number of eosinophils in the fluid was significantly lower in the rats fed the raffinose diet than in those fed the control diet. Dietary raffinose significantly reduced IL-4 and IL-5 mRNA levels in lung tissue and tended to lower ovalbumin-specific Ig E levels. Suppression of eosinophilia by dietary raffinose was still observed in caecectomised and neomycin-administered rats, suggesting little contribution by the colonic bacteria to the effect of raffinose. Intraperitoneal administration of raffinose also suppressed eosinophilia. Significant concentrations of raffinose were detected in portal venous and abdominal arterial plasma after the intragastric administration of raffinose. Overall, the findings suggest that dietary raffinose ameliorates allergic airway eosinophilia at least partly via post-absorptive mechanisms in Brown Norway rats.

scholarly journals Macrophage expression and prognostic significance of the long pentraxin PTX3 in COVID-19

2020 ◽  
Author(s):  
Enrico Brunetta ◽  
Marco Folci ◽  
Barbara Bottazzi ◽  
Maria De Santis ◽  
Alessandro Protti ◽  
...  
Keyword(s):  
Single Cell ◽  
Plasma Levels ◽  
Mononuclear Cells ◽  
Cox Regression ◽  
Single Cell Analysis ◽  
Vascular Endothelial Cells ◽  
Prognostic Significance ◽  
Lavage Fluid ◽  
Prognostic Indicator ◽  
Vascular Pathology

ABSTRACTPTX3 is an essential component of humoral innate immunity, involved in resistance to selected pathogens and in the regulation of inflammation. PTX3 plasma levels are associated with poor outcome in systemic inflammatory conditions and vascular pathology. The present study was designed to assess expression and significance of PTX3 in COVID-19. By bioinformatics analysis of public databases PTX3 expression was detected in lung respiratory cell lines exposed to SARS-CoV-2. By analysis at single cell level of COVID-19 circulating mononuclear cells, we found that PTX3 was selectively expressed by monocytes among circulating leukocytes. Moreover, in lung bronchoalveolar lavage fluid, single cell analysis revealed selective expression of PTX3 in neutrophils and macrophages, which play a major role in the pathogenesis of the disease. By immunohistochemistry, PTX3 was expressed by lung myelomocytic cells, type 2 pneumocytes and vascular endothelial cells. PTX3 plasma levels were determined by ELISA in 96 consecutive patients with a laboratory-confirmed diagnosis of COVID-19. Higher PTX3 plasma levels were observed in 52 (54.2%) patients admitted in ICU (median 21.0ng/mL, IQT 15.5-46.3 vs 12.4ng/mL IQT 6.1-20.2 in ward patients; p=0.0017) and in 22 (23%) patients died by 28 days (39.8ng/mL, IQT 20.2-75.7 vs 15.7ng/mL, IQT 8.2-21.6 in survivors; p=0.0001). After determining an optimal PTX3 cut-off for the primary outcome, the Kaplan-Meier curve showed an increased mortality in patients with PTX3>22.25ng/mL (Log-rank tests p<0.0001). In Cox regression model, PTX3>22.25ng/mL showed an adjusted Hazard Ratio (aHR) of 7.6 (95%CI2.45-23.76) in predicting mortality. Performing a multivariate logistic regression including all inflammatory markers (PTX3, ferritin, D-Dimer, IL-6, and CRP), PTX3 was the only marker significantly associated with death (aHR 1.13;95%CI1.02-1.24; p=0.021). The results reported here suggest that circulating and lung myelomonocytic cells are a major source of PTX3 and that PTX3 plasma levels can serve as a strong prognostic indicator of short-term mortality in COVID-19.

A mesoporous organosilica grafted Pd catalyst (MOG-Pd) for efficient base free and phosphine free synthesis of tertiary butyl esters via tertiary-butoxycarbonylation of boronic acid derivatives without using carbon monoxide

2015 ◽  
Vol 17 (6) ◽  
pp. 3540-3551 ◽  
Author(s):  
Kajari Ghosh ◽  
Rostam Ali Molla ◽  
Md. Asif Iqubal ◽  
S. M. Islam
Keyword(s):  
Carbon Monoxide ◽  
Boronic Acid ◽  
High Efficiency ◽  
Pd Catalyst ◽  
Tertiary Butyl ◽  
Butyl Esters ◽  
Mesoporous Organosilica ◽  
Green Condition ◽  
Boronic Acid Derivatives

A reusable MOG-Pd catalyst has been synthesized, characterized and it shows high efficiency in tert-butoxycarbonylation under green condition.

scholarly journals Melatonin Alleviates Radiation-Induced Lung Injury via Regulation of miR-30e/NLRP3 Axis

2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Xu Wu ◽  
Haiying Ji ◽  
Yuli Wang ◽  
Chenlin Gu ◽  
Wenyu Gu ◽  
...  
Keyword(s):  
Lung Injury ◽  
Nlrp3 Inflammasome ◽  
Intraperitoneal Administration ◽  
Lavage Fluid ◽  
Raw 264.7 Cells ◽  
Luciferase Reporter ◽  
Pcr Analysis ◽  
Inflammasome Activation ◽  
Caspase 1 ◽  
Radiation Induced

Melatonin is a well-known anti-inflammatory and antioxidant molecule, which plays a crucial role in various physiological functions. In this study, mice received a single dose of 15 Gy radiation delivered to the lungs and daily intraperitoneal administration of melatonin. After 7 days, mice were processed to harvest either bronchoalveolar lavage fluid for cytokine assays or lungs for flow cytometry and histopathological studies. Herein, we showed that melatonin markedly alleviated the oxidative stress and injury, especially suppressing the infiltration of macrophages (CD11b+CD11c−) and neutrophils (CD11b+Ly6G+) to the irradiated lungs. Moreover, in the irradiated RAW 264.7 cells, melatonin blocked the NLRP3 inflammasome activation accompanied with the inhibition of the IL-1β release and caspase-1 activity. However, melatonin restored the downregulated miR-30e levels. Quantitative PCR analysis of miR-30e and NLRP3 indicated the negative correlation between them. Notably, immunofluorescence staining showed that overexpression of miR-30e dramatically diminished the increased NLRP3 expression. Luciferase reporter assay confirmed that NLRP3 was a target gene of miR-30e. Western blotting revealed that transfection with miR-30e mimics markedly reduced the expressions of NLRP3 and cleaved caspase-1, whereas this phenomenon was reversed by the miR-30e inhibitor. Consistent with this, the beneficial effect of melatonin under irradiated exposure was blunted in cells transfected with anti-miR-30e. Collectively, our results demonstrate that the NLRP3 inflammasome contributed to the pathogenesis of radiation-induced lung injury. Meanwhile, melatonin exerted its protective effect through negatively regulating the NLRP3 inflammasome in macrophages. The melatonin-mediated miR-30e/NLRP3 signaling may provide novel therapeutic targets for radiation-induced injury.

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