Effect of cigarette-smoke condensates on homografts of embryonic lung tissue in rats

1963 ◽  
Vol 86 (1) ◽  
pp. 199-207 ◽  
Author(s):  
Lee-Tsün Hou ◽  
R. A. Willis
Keyword(s):  
Cigarette Smoke ◽  
Lung Tissue ◽  
Embryonic Lung

Effect of cigarette-smoke condensates on homografts of embryonic lung tissue in rats

1964 ◽  
Vol 2 (3) ◽  
pp. 442
Author(s):  
L. T. Hou ◽  
R. A. Willis
Keyword(s):  
Cigarette Smoke ◽  
Lung Tissue ◽  
Embryonic Lung

scholarly journals COLLAGEN BIOSYNTHESIS

1957 ◽  
Vol 3 (5) ◽  
pp. 685-695 ◽  
Author(s):  
J. Frederick Woessner ◽  
Bernard S. Gould
Keyword(s):  
Ascorbic Acid ◽  
Cell Growth ◽  
Lung Tissue ◽  
Appreciable Effect ◽  
Collagen Biosynthesis ◽  
Embryonic Lung ◽  
Marked Contrast ◽  
Collagen Formation ◽  
Quantitative Studies ◽  
Total Failure

Quantitative studies of collagen formation by chick embryonic lung tissue grown in media deficient in, or completely lacking, ascorbic acid have been carried out. Cell growth and collagen formation in such cultures can proceed almost normally in media lacking ascorbic acid. Ascorbic acid in combination with whole embryo extract, dialyzed media, or synthetic mixture number 703 was found to have no appreciable effect on cell growth or total collagen formation. This is in marked contrast to the almost total failure of collagen formation in scorbutic animals and suggests that for slow collagen biosynthesis as distinct from more prolific collagen-producing systems, ascorbic acid plays an indirect role.

Action of allogeneic serum from a pregnant pneumonectomized rat on embryonic lung tissue

1978 ◽  
Vol 86 (1) ◽  
pp. 931-935
Author(s):  
I. I. Orlova ◽  
N. G. Lisatova ◽  
S. D. Mikhal'chenko
Keyword(s):  
Lung Tissue ◽  
Embryonic Lung

scholarly journals Cigarette smoke alters the transcriptome of non-involved lung tissue in lung adenocarcinoma patients

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Giulia Pintarelli ◽  
Sara Noci ◽  
Davide Maspero ◽  
Angela Pettinicchio ◽  
Matteo Dugo ◽  
...  
Keyword(s):  
Gene Expression ◽  
Lung Adenocarcinoma ◽  
Cigarette Smoke ◽  
Lung Tissue ◽  
Gene Networks ◽  
Lung Parenchyma ◽  
Fold Change ◽  
Differentially Expressed ◽  
Significant Gene ◽  
Never Smokers

Abstract Alterations in the gene expression of organs in contact with the environment may signal exposure to toxins. To identify genes in lung tissue whose expression levels are altered by cigarette smoking, we compared the transcriptomes of lung tissue between 118 ever smokers and 58 never smokers. In all cases, the tissue studied was non-involved lung tissue obtained at lobectomy from patients with lung adenocarcinoma. Of the 17,097 genes analyzed, 357 were differentially expressed between ever smokers and never smokers (FDR < 0.05), including 290 genes that were up-regulated and 67 down-regulated in ever smokers. For 85 genes, the absolute value of the fold change was ≥2. The gene with the smallest FDR was MYO1A (FDR = 6.9 × 10−4) while the gene with the largest difference between groups was FGG (fold change = 31.60). Overall, 100 of the genes identified in this study (38.6%) had previously been found to associate with smoking in at least one of four previously reported datasets of non-involved lung tissue. Seven genes (KMO, CD1A, SPINK5, TREM2, CYBB, DNASE2B, FGG) were differentially expressed between ever and never smokers in all five datasets, with concordant higher expression in ever smokers. Smoking-induced up-regulation of six of these genes was also observed in a transcription dataset from lung tissue of non-cancer patients. Among the three most significant gene networks, two are involved in immunity and inflammation and one in cell death. Overall, this study shows that the lung parenchyma transcriptome of smokers has altered gene expression and that these alterations are reproducible in different series of smokers across countries. Moreover, this study identified a seven-gene panel that reflects lung tissue exposure to cigarette smoke.

The structure of long-surviving homografts of embryonic lung tissue in rats

1964 ◽  
Vol 2 (4) ◽  
pp. 576
Author(s):  
R. A. Willis ◽  
L. T. Hou
Keyword(s):  
Lung Tissue ◽  
Embryonic Lung

scholarly journals AP-2α expression and cell apoptosis of the lung tissue of rats with COPD and ECV304 cells stimulated by cigarette smoke extract

2011 ◽  
Vol 56 (15) ◽  
pp. 1562-1568 ◽  
Author(s):  
JunLi Li ◽  
Yan Chen ◽  
Ping Chen ◽  
Shan Cai ◽  
Hong Peng ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Lung Tissue ◽  
Cell Apoptosis ◽  
Cigarette Smoke Extract

Humic-like substances in cigarette smoke condensate and lung tissue of smokers

1994 ◽  
Vol 266 (4) ◽  
pp. L382-L388 ◽  
Author(s):  
A. J. Ghio ◽  
J. Stonehuerner ◽  
D. R. Quigley
Keyword(s):  
Free Radical ◽  
Cigarette Smoke ◽  
Lung Tissue ◽  
Cigarette Smoke Exposure ◽  
Cigarette Smoke Condensate ◽  
Free Radical Generation ◽  
Carboxylate Content ◽  
Radical Generation

Deposition of pigmented matter in the lower respiratory tract correlates with the extent of emphysema in smokers as well as with free radical generation and iron accumulation. Pulmonary emphysema is postulated to be mediated by free radical generation which is either directly or indirectly associated with cigarette smoke exposure. The hypothesis was tested that 1) incomplete combustion of tobacco yields humic-like substances (HLS) which 2) deposit in the lung as pigmented particulates, 3) complex iron cations in vitro and in vivo, and 4) have a capacity to catalyze oxidant formation. HLS, isolated by alkali extraction of cigarette smoke condensate (CSC) (Tobacco Health Research Institute, University of Kentucky), demonstrated a high carbon and low carboxylate content on elemental and functional group analyses, respectively, compared with values for HLS sequestered from soils. The HLS isolated from CSC had a capacity to complex iron in vitro and accumulated the metal in vivo after intratracheal instillation in an animal model. Both HLS and its iron complex generated free radicals, and some portion of this oxidant generation was metal dependent. Lung tissue collected at autopsy from smokers contained HLS with an infrared spectrum almost identical to that of the material isolated from CSC. Associations between particulate deposition, metal accumulation, and free radical generation suggest a possible role of HLS in the induction of lung disease following cigarette exposure.

scholarly journals The time pattern of selenomethionine administration in preventing free radicals due to exposure to electric cigarette smoke

2021 ◽  
Vol 10 (2) ◽  
Author(s):  
Rivan Virlando Suryadinata ◽  
Bambang Wirjatmadi ◽  
Amelia Lorensia
Keyword(s):  
Free Radicals ◽  
Cigarette Smoke ◽  
Lung Tissue ◽  
Cell Damage ◽  
Control Group ◽  
Early Application ◽  
Control Group Design ◽  
Time Pattern ◽  
Negative Effect ◽  
Male Wistar Rats

Background: Most people believe that electric cigarettes have no negative effect on health,  which causes them to use it more. However, exposure to the smoke from these cigarettes is bad for the health and causes cell damage. Antioxidants play an important role in preventing cell damage, and they can be obtained through the oral administration of selenomethionine.Design and methods: This study used an experimental method and a post-test control group design. Male Wistar rats, which were exposed to cigarette smoke were given selenomethionine orally and then tested for the presence of free radicals. The measurement of lung tissue damage was conducted by assessing the level of malondialdehyde in the blood and immunohistochemistry (IHC) of the lung tissue.Result: The study showed that differences in the time of administration of selenomethionine affect the levels of malondialdehyde in the blood and expression of malondialdehyde in the lung tissue (p<0.05). Consequently, the two groups showed a strong (r=0.861) and significant (p=0.000) relationship with each other.Conclusion: The early application of selenomethionine can prevent increased levels of malondialdehyde in the blood and lung tissue due to exposure to e-cigarette smoke.

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