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7 records – page 1 of 1.

Effect of administration of lead nitrate to pregnant rats on the lungs in their offspring.

https://arctichealth.org/en/permalink/ahliterature63150
Source
Bull Exp Biol Med. 2005 Jun;139(6):655-7
Publication Type
Article
Date
Jun-2005
Author
O A Lebed'ko
B Ya Ryzhavskii
Author Affiliation
Clinical and Diagnostic Laboratory, Khabarovsk Branch, Far-Eastern Research Center for Physiology and Pathology of Respiration, Siberian Division of the Russian Academy of Medical Sciences, Russia.
Source
Bull Exp Biol Med. 2005 Jun;139(6):655-7
Date
Jun-2005
Language
English
Publication Type
Article
Keywords
Animals
Comparative Study
Female
Lead - administration & dosage - toxicity
Lung - drug effects - metabolism - physiology
Lung Diseases - chemically induced - metabolism - pathology - physiopathology
Lung Volume Measurements
Nitrates - administration & dosage - toxicity
Oxidation-Reduction
Pregnancy
Prenatal Exposure Delayed Effects
Pulmonary Alveoli - drug effects - metabolism
Rats
Reactive Oxygen Species - metabolism
Abstract
Lead nitrate in a dose of 200 mg/kg was administered to female rats via a gartric tube on days 5 and 12 of pregnancy. The lungs of their offspring were examined on day 40 of life. We found a decrease in the ratio between the specific volumes of alveolar lumens and interalveolar septa and hypertrophy of lymphoid tissue in the bronchial wall (compared to the offspring of intact females). Chemiluminescent analysis revealed activation of lipid peroxidation and decrease in antioxidant antiradical activity of the lungs.
PubMed ID
16224572 View in PubMed
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Effects of cyclosporin A administered into the airways against antigen-induced airway inflammation and hyperreactivity in the rat.

https://arctichealth.org/en/permalink/ahliterature15481
Source
Eur J Pharmacol. 2001 May 25;420(2-3):165-73
Publication Type
Article
Date
May-25-2001
Author
S L Underwood
S. McMillan
R. Reeves
J. Hunt
C J Brealey
S. Webber
M. Foster
C A Sargent
Author Affiliation
Aventis Pharma, Pharmacology Department, Dagenham Research Centre, Rainham Road South, Essex RM10 7XS, Dagenham, UK. stephen.underwood@aventis.com
Source
Eur J Pharmacol. 2001 May 25;420(2-3):165-73
Date
May-25-2001
Language
English
Publication Type
Article
Keywords
Administration, Inhalation
Animals
Antigens - administration & dosage
Antigens, CD2 - analysis
Antigens, CD4 - analysis
Area Under Curve
Bronchial Hyperreactivity - chemically induced - genetics - prevention & control
Bronchitis - chemically induced - immunology - prevention & control
Cyclosporine - pharmacokinetics - pharmacology
Dose-Response Relationship, Drug
Eosinophils - pathology
Immunosuppressive Agents - pharmacokinetics - pharmacology
Interleukin-5 - genetics
Lung - drug effects - metabolism - pathology
Lymphocytes - drug effects - immunology - pathology
Male
RNA, Messenger - drug effects - genetics - metabolism
Rats
Rats, Inbred BN
Rats, Sprague-Dawley
Receptors, Interleukin-2 - analysis
Abstract
The immunosuppressant cyclosporin A given orally has anti-asthma properties but carries an undesirable risk of systemic effects. We administered cyclosporin A to Brown Norway rats either orally (p.o.) or topically by intratracheal (i.t.) instillation into the airways before inhaled antigen. Cyclosporin A suppressed the antigen-induced accumulation of activated (CD25+) CD4+ T lymphocytes and eosinophils in the lung, interleukin-5 mRNA expression in lung tissue and airway hyperreactivity. Intratracheal cyclosporin A suppressed cell accumulation at a 10-fold lower dose than that required orally. Minimum effective doses were 3 mg x kg(-1) i.t. and 30 mg x kg(-1) p.o. Intratracheal administration reduced the plasma concentration and systemic exposure compared with an equieffective oral dose, but the reduction (4-5-fold) was not as large as anticipated. Our data suggests that although topical administration to asthmatics would provide some potential for an improved safety margin, it may not offer any major advantage over existing oral therapy. However, the data clearly demonstrate that a novel immunosuppressant with similar anti-inflammatory properties but reduced potential for systemic effects would offer an attractive therapy for severe asthma.
PubMed ID
11408039 View in PubMed
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Evaluation of the health risk associated with exposure to chloroform in indoor swimming pools.

https://arctichealth.org/en/permalink/ahliterature196697
Source
J Toxicol Environ Health A. 2000 Oct 27;61(4):225-43
Publication Type
Article
Date
Oct-27-2000
Author
B. Lévesque
P. Ayotte
R. Tardif
G. Charest-Tardif
E. Dewailly
D. Prud'Homme
G. Gingras
S. Allaire
R. Lavoie
Author Affiliation
Unité de recherche en santé publique, Centre hospitalier universitaire de Québec, Beauport, Canada. blevesque@cspq.qc.ca
Source
J Toxicol Environ Health A. 2000 Oct 27;61(4):225-43
Date
Oct-27-2000
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Air Pollutants - adverse effects - pharmacokinetics
Air Pollution, Indoor - adverse effects
Child
Chloroform - adverse effects - pharmacokinetics
Environmental Monitoring - methods
Female
Humans
Linear Models
Lung - drug effects - metabolism
Male
Middle Aged
Neoplasms - chemically induced
Quebec
Risk assessment
Skin Absorption
Swimming
Swimming Pools - standards
Abstract
The exposure of swimmers to chloroform (CHCl3) was investigated in indoor swimming pools of the Quebec City region along with the associated carcinogenic risk. Six training sessions involving 52 competition swimmers (11 to 20 yr old) were conducted in 3 different pools, while 12 adult leisure swimmers attended 5 sessions, each held in a different pool. For each session, water and ambient air CHCl3 concentrations were measured and CHCl3 levels in alveolar air samples (CHCl3 ALV) collected from swimmers prior to entering the swimming pool premises and after 15, 35, and 60 min of swimming. Mean water concentrations varied from 18 microg/L to 80 microg/L, while those in air ranged from 78 microg/m3 to 329 microg/m3. Multiple linear regression analyses revealed that CHCl3 ALV values in competition swimmers were strongly correlated to ambient air and water levels, and to a lesser degree to the intensity of training. Only ambient air concentration was positively correlated to CHCl3 ALV in the leisure group. Concentrations of CHCl3 metabolites bound to hepatic and renal macromolecules, estimated using a physiologically based pharmacokinetic (PBPK) model, were 1.6 and 1.9 times higher for the competition swimmers than for the leisure swimmers, respectively. The highest hepatic concentration predicted in competition swimmers, 0.22 microg CHCl3 equivalents/kg of tissue, was at least 10,000 times lower than the smallest no observed effect level for liver tumors in animals. Data indicate that the safety margin is therefore very large, for competitive swimmers as well as for leisure swimmers.
PubMed ID
11071317 View in PubMed
Less detail

Mice exposed in situ to urban air pollution exhibit pulmonary alterations in gene expression in the lipid droplet synthesis pathways.

https://arctichealth.org/en/permalink/ahliterature115173
Source
Environ Mol Mutagen. 2013 May;54(4):240-9
Publication Type
Article
Date
May-2013
Author
Andrea Rowan-Carroll
Sabina Halappanavar
Andrew Williams
Christophers M Somers
Carole L Yauk
Author Affiliation
Environmental Health Science and Research Bureau, Health Canada, Ottawa, Ontario, Canada.
Source
Environ Mol Mutagen. 2013 May;54(4):240-9
Date
May-2013
Language
English
Publication Type
Article
Keywords
Air Pollutants - toxicity
Air Pollution
Animals
Biosynthetic Pathways - genetics
DNA Adducts - metabolism
DNA Breaks
Humans
Industrial Waste
Lipid Metabolism - drug effects - genetics
Lung - drug effects - metabolism
Lung Diseases - chemically induced
Male
Mice
Mice, Inbred C57BL
Oligonucleotide Array Sequence Analysis
Ontario
Particulate Matter - toxicity
Real-Time Polymerase Chain Reaction
Spermatozoa - drug effects
Transcriptome - drug effects
Urban Population
Abstract
It is clear that particulate air pollution poses a serious risk to human health; however, the underlying mechanisms are not completely understood. We investigated pulmonary transcriptional responses in mice following in-situ exposure to ambient air in a heavily industrialized urban environment. Mature C57BL/CBA male mice were caged in sheds near two working steel mills and a major highway in Hamilton, Ontario, Canada in the spring/summer of 2004. Control mice were housed in the same environment, but received only high-efficiency particle filtered air (HEPA). Whole lung tissues were collected from mice exposed for 3, 10, or for 10 weeks followed by 6 weeks recovery in the laboratory (16 weeks). DNA microarrays were used to profile changes in pulmonary gene expression. Transcriptional profiling revealed changes in the expression of genes implicated in the lipid droplet synthesis (Plin I, Dgat2, Lpl, S3-12, and Agpat2), and antioxidant defense (Ucp1) pathways in mice breathing unfiltered air. We postulate that exposure to urban air, containing an abundance of particulate matter adsorbed with polycyclic aromatic hydrocarbons, triggers lipid droplet (holding depots for lipids and malformed/excess proteins tagged for degradation) synthesis in the lungs, which may act to sequester particulates. Increased lipid droplet synthesis could lead to endogenous/stressor-induced production of reactive oxygen species and activation of antioxidant mechanisms. Further investigation into the stimulation of lipid droplet synthesis in the lung in response to air pollution and the resulting health implications is warranted.
PubMed ID
23536514 View in PubMed
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A novel transcription factor inhibitor, SP100030, inhibits cytokine gene expression, but not airway eosinophilia or hyperresponsiveness in sensitized and allergen-exposed rat.

https://arctichealth.org/en/permalink/ahliterature15448
Source
Br J Pharmacol. 2001 Nov;134(5):1029-36
Publication Type
Article
Date
Nov-2001
Author
T J Huang
I M Adcock
K F Chung
Author Affiliation
Thoracic Medicine, Chang Gung Memorial Hospital, Keelung Branch, Taiwan, Republic of China.
Source
Br J Pharmacol. 2001 Nov;134(5):1029-36
Date
Nov-2001
Language
English
Publication Type
Article
Keywords
Allergens - immunology
Animals
Antigens, CD2 - analysis
Antigens, CD4 - analysis
Antigens, CD8 - analysis
Blotting, Western
Bronchial Hyperreactivity - genetics - immunology - prevention & control
Bronchoalveolar Lavage Fluid - cytology
Cytokines - genetics
Eosinophils - cytology - drug effects - immunology
Gene Expression Regulation - drug effects
Immunohistochemistry
Immunosuppressive Agents - pharmacology
Interferon Type II - genetics
Interleukin-10 - genetics
Interleukin-2 - genetics
Interleukin-4 - genetics
Interleukin-5 - genetics
Lung - drug effects - metabolism
Lymphocytes - cytology - drug effects - immunology
Macrophages - cytology - drug effects - immunology
Male
NF-kappa B - antagonists & inhibitors
Neutrophils - cytology - drug effects - immunology
Organic Chemicals
Ovalbumin - immunology
Proto-Oncogene Proteins c-jun - drug effects - metabolism
Pulmonary Eosinophilia - genetics - immunology - prevention & control
RNA, Messenger - drug effects - genetics - metabolism
Rats
Rats, Inbred BN
Respiratory Mucosa - drug effects - immunology - pathology
Specific Pathogen-Free Organisms
Transcription Factor AP-1 - antagonists & inhibitors
Transcription Factors - antagonists & inhibitors
Abstract
1. We examined the effect of SP100030, a novel inhibitor of activator protein-1 (AP-1) and nuclear factor (NF)-kappa B transcription factors, in a rat model of asthma. 2. Sensitized Brown-Norway rats were treated with SP100030 (20 mg kg(-1) day(-1) for 3 days) intraperitoneally prior to allergen challenge. Allergen exposure of sensitized rats induced bronchial hyperresponsiveness (BHR), accumulation of inflammatory cells in bronchoalveolar lavage (BAL) fluid, and also an increase in eosinophils and CD2(+), CD4(+) and CD8(+) T-cells in the airways together with mRNA expression for IL-2, IL-4, IL-5, IL-10, and IFN-gamma. 3. Pre-treatment with SP100030 inhibited BAL lymphocyte influx (P
PubMed ID
11682451 View in PubMed
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[N-stearoylethanolamine inhibits growth and metastasis of the Lewis carcinoma and modulates lipid composition of the lung during tumorogenesis in mice]

https://arctichealth.org/en/permalink/ahliterature79532
Source
Ukr Biokhim Zh. 2006 Jan-Feb;78(1):135-42
Publication Type
Article
Author
Hula N M
Khmel' T O
Klimashevs'kyi V M
Kulik H I
Todor I M
Source
Ukr Biokhim Zh. 2006 Jan-Feb;78(1):135-42
Language
Ukrainian
Publication Type
Article
Keywords
Animals
Carcinoma, Lewis Lung - drug therapy - metabolism - pathology
Ethanolamines - pharmacology - therapeutic use
Fatty Acids - chemistry - metabolism
Lipid Metabolism - drug effects
Lipid Peroxidation - drug effects
Lung - drug effects - metabolism - pathology
Male
Mice
Mice, Inbred C57BL
Neoplasm Metastasis
Phospholipids - chemistry - metabolism
Stearic Acids - pharmacology - therapeutic use
Abstract
We investigated the influence of N-stearoylethanolamine (NSE) on tumor growth and metastasis of the lung Lewis carcinoma in mice. The effect of NSE on lipid composition of lung tissue under tumorogenesis was also studied. We demonstrated that NSE inhibited the tumor growth and decreased the volume and quantity of metastases being administered from the fourth day after injection of tumor cells to the last day of experiment and being administrated from the 21th day after injection of tumor cells to the last day of the experiment. The analysis of the lipid composition of the lung tissue showed the decrease of total phospholipid levels and change of the phospholipid spectra under tumor growth. The decreasing of the concentration of phosphatidylcholine, sphyngomyeline, phosphatidylserine and lysophosphatidylcholine in the lung tissue of tumor-bearding mice in comparison with lung of intact animals was observed. It was found that administration of NSE increased the level of lysophosphatidylcholine and decreased the concentration of phosphatidylinositol in investigated tissues. The content of sphingosine was increased in lung tissue of mice fed by NSE in comparison with tumor-bearing mice. The carcinoma development was associated by the significant decreasing of cholesterol level and by the increasing of unsaturated fatty acids in membrane phospholipids. The amount of the tiobarbituric acid (TBA) reactive substances in tumor-bearing mice was elevated. The administration of NSE inhibited the accumulation of TBA reacting compounds.
PubMed ID
17147277 View in PubMed
Less detail

Repeated allergen exposure of sensitized Brown-Norway rats induces airway cell DNA synthesis and remodelling.

https://arctichealth.org/en/permalink/ahliterature15632
Source
Eur Respir J. 1999 Sep;14(3):633-41
Publication Type
Article
Date
Sep-1999
Author
M. Salmon
D A Walsh
H. Koto
P J Barnes
K F Chung
Author Affiliation
Thoracic Medicine, Imperial College School of Medicine at the National Heart and Lung Institute, London, UK.
Source
Eur Respir J. 1999 Sep;14(3):633-41
Date
Sep-1999
Language
English
Publication Type
Article
Keywords
Actins - metabolism
Allergens - pharmacology
Animals
Antigens, CD2 - metabolism
Asthma - chemically induced - metabolism - pathology
Blood Proteins - metabolism
Bromodeoxyuridine - metabolism
Bronchial Hyperreactivity - chemically induced - metabolism - pathology
Comparative Study
DNA - biosynthesis
Disease Models, Animal
Eosinophil Granule Proteins
Eosinophils - metabolism - pathology
Epithelial Cells - metabolism - pathology
Lung - drug effects - metabolism - pathology
Male
Muscle, Smooth - metabolism - pathology
Ovalbumin - pharmacology
Rats
Rats, Inbred BN
Research Support, Non-U.S. Gov't
Ribonucleases
T-Lymphocytes - metabolism - pathology
Abstract
Chronic inflammation in asthmatic airways can lead to characteristic airway smooth muscle (ASM) thickening and pathological changes within the airway wall. This study assessed the effect of repeated allergen exposure on ASM and epithelial cell deoxyribonucleic acid (DNA) synthesis, cell recruitment and airway wall pathology. Brown-Norway rats were sensitized and then exposed to ovalbumin or saline aerosol every 3 days on six occasions. After the final exposure, rats were administered twice daily for 7 days with the DNA S-phase marker bromodeoxyuridine (BrdU). Using a triple immunohistochemical staining technique, BrdU incorporation into ASM and epithelium was quantified employing computer-assisted image analysis. There were >3-fold mean increases in BrdU incorporation into ASM from 1.3% of cells (95% confidence interval (CI) 1.0-1.6) in saline controls to 4.7% (95% CI 2.6-6.7) after allergen exposure (p
PubMed ID
10543287 View in PubMed
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7 records – page 1 of 1.