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Journal articles on the topic 'Lung Neoplasms/chemically induced'

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Published: 2 June 2025

Last updated: 31 July 2025

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1

Gunning, W. T., G. D. Stoner, and P. J. Goldblatt. "Ultrastructural observations of lung neoplasms induced in the strain A/J mouse by benzo(a)pyrene and ethylnitrosourea." Proceedings, annual meeting, Electron Microscopy Society of America 45 (August 1987): 854–55. http://dx.doi.org/10.1017/s0424820100128559.

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The current literature regarding the histogenesis of mouse lung adenomas suggests two alternative cells of origin for these tumors. The Type II pneumocyte was accepted by most investigators as the cell which proliferated either spontaneously or by chemical induction, until Kauffman and co-workers reported histologic and ultrastructural features of a Clara cell adenoma, and indicated that in Swiss mice, 63% of all chemically induced tumors appeared to be Clara cell derived. Ward et al. using immunocytochemical techniques have demonstrated that all lung adenomas they tested in B6C3F1, BALB, and

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2

Dixon, Darlene, and Robert R. Maronpot. "Histomorphologic Features of Spontaneous and Chemically-Induced Pulmonary Neoplasms in B6C3F1 Mice and Fischer 344 Rats." Toxicologic Pathology 19, no. 4_part_1 (1991): 540–56. http://dx.doi.org/10.1177/0192623391019004-119.

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The histomorphologic features of spontaneous and chemically-induced lung neoplasms in male and female B6C3F1 mice and Fischer 344 rats are described. Primary pulmonary neoplasms in mice and rats were classified as alveolar/bronchiolar (A/B) adenoma or carcinoma (including variants with squamous and mucinous cell differentiation), bronchial adenoma or carcinoma, squamous cell carcinoma or mesenchymal tumors. A/B adenomas and carcinomas were the most common spontaneous pulmonary neoplasms observed in both mice and rats, but were observed less frequently in rats. In the National Toxicology Progra

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3

Ton, Thai-Vu T., Hue-Hua L. Hong, Colleen H. Anna, et al. "Predominant K-ras Codon 12 G → A Transition in Chemically Induced Lung Neoplasms in B6C3F1 Mice." Toxicologic Pathology 32, no. 1 (2004): 16–21. http://dx.doi.org/10.1080/01926230490260682.

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4

Karabela, Sophia, Ioannis Psallidas, Taylor Sherrill та ін. "Opposing effects of bortezomib-induced nuclear factor-κB inhibition on chemical lung carcinogenesis." Carcinogenesis 33, № 4 (2012): 859–67. https://doi.org/10.1093/carcin/bgs024.

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Since recent evidence indicates a requirement for epithelial nuclear factor (NF)-κB signaling in lung tumorigenesis, we investigated the impact of the NF-κB inhibitor bortezomib on lung tumor promotion and growth. We used an experimental model in which wild-type mice or mice expressing an NF-κB reporter received intraperitoneal urethane (1 g/kg) followed by twice weekly bortezomib (1 mg/kg) during distinct periods of tumor initiation/progression. Mice were serially assessed for lung NF-κB activation, inflammation and carcinogenesis. Short-term proteasome inhibition with bortezomib did not impa

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5

Tanaka, Takuji, Takahiro Tanaka, Mayu Tanaka та Toshiya Kuno. "Cancer Chemoprevention by Citrus Pulp and Juices Containing High Amounts ofβ-Cryptoxanthin and Hesperidin". Journal of Biomedicine and Biotechnology 2012 (2012): 1–10. http://dx.doi.org/10.1155/2012/516981.

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β-Cryptoxanthin, a carotenoid, and hesperidin, a flavonoid, possess inhibitory effects on carcinogenesis in several tissues. We recently have prepared a pulp (CHRP) and citrus juices (MJ2 and MJ5) from a satsuma mandarin (Citrus unshiuMar.) juice (MJ). They contain high amounts ofβ-cryptoxanthin and hesperidin. We have demonstrated that CHRP and/or MJs inhibit chemically induced rat colon, rat tongue, and mouse lung tumorigenesis. Gavage with CHRP resulted in an increase of activities of detoxifying enzymes in the liver, colon, and tongue rats'. CHRP and MJs were also able to suppress the expr

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6

Ogawa, Kumiko, Katsumi Imaida, Tsuneo Masui, et al. "Chemically induced lung and forestomach neoplasias in transgenic mice carry mutant forms of the human c-Ha-ras transgene." Carcinogenesis 17, no. 2 (1996): 341–45. http://dx.doi.org/10.1093/carcin/17.2.341.

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7

Karabela, Sophia, Chrysoula Kairi, Sophia Magkouta, et al. "Neutralization of tumor necrosis factor bioactivity ameliorates urethane-induced pulmonary oncogenesis in mice." Neoplasia (New York, N.Y.) 13, no. 12 (2011): 1143–51. https://doi.org/10.1593/neo.111224.

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Tumor necrosis factor (TNF) has been implicated in inflammation-associated tumor progression. Although multiple reports identified a role for TNF signaling in established cancers, few studies have assessed the impact of TNF blockade on early tumor formation promotion. We aimed at exploring the effects of TNF neutralization in a preclinical mouse model of lung carcinogenesis. For this, Balb/c mice (n = 42) received four weekly intraperitoneal urethane injections (1 g/kg) and twice-weekly intraperitoneal soluble TNF receptor (etanercept; 10 mg/kg) administered during tumor initiation/promotion,

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8

Wang, Min, Theodora R. Devereux, Haris G. Vikis та ін. "Pol ι Is a Candidate for the Mouse Pulmonary Adenoma Resistance 2 Locus, a Major Modifier of Chemically Induced Lung Neoplasia". Cancer Research 64, № 6 (2004): 1924–31. http://dx.doi.org/10.1158/0008-5472.can-03-3080.

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9

Maydin, M. A., M. N. Yurova, E. I. Fedoros, et al. "Effect of inactivating heterozygous mutations in DNA repair genes on experimental lung carcinogenesis in mice." Russian Journal of Biotherapy 23, no. 1 (2024): 37–44. http://dx.doi.org/10.17650/1726-9784-2024-23-1-37-44.

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Background. Inactivating mutations in Chek2 and Gprc5a genes are known to be associated with cancer development. Experimental carcinogenesis studies in genetically modified mice generate new data on their influence on pathology development.Aim. In the present study in a model of lung carcinogenesis, survival parameters as well as tumor multiplicity and size in mice with Chek2 and Gprc5a heterozygous inactivating mutations were evaluated.Material and methods. F2 hybrid mice from crosses between CBAB6F1 males heterozygous for the studied mutations and wild-type BALB / c females were used: Chek2d

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10

Green, John. "Chemically Induced Lung Sensitisation." Indoor and Built Environment 3, no. 3 (1994): 166–67. http://dx.doi.org/10.1159/000463547.

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11

Johnson, G. Allan, and Robert R. Maronpot. "Magnetic Resonance Microscopy of Chemically-Induced Liver Foci." Toxicologic Pathology 17, no. 4_part_1 (1989): 613–16. http://dx.doi.org/10.1177/0192623389017004106.

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Magnetic resonance imaging (MRI) is a new imaging technique used in clinical diagnosis. This paper describes extension of the technique to basic research applications–specifically detecting and characterizing chemically-induced liver neoplasms and foci of cellular alteration. Two systems have been built that allow spatial microscopic resolution–more than 100,000 x greater than that of earlier efforts. Use of spin-lattice (T1) and spin-spin (T2) relaxation times permits detailed characterization of the tissue.

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12

Vikis, Haris G. "Mouse models of chemically-induced lung carcinogenesis." Frontiers in Bioscience E5, no. 3 (2013): 939–46. http://dx.doi.org/10.2741/e673.

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13

Wechsler, Richard J., Robert M. Steiner, and Emily F. Conant. "OCCUPATIONALLY INDUCED NEOPLASMS OF THE LUNG AND PLEURA." Radiologic Clinics of North America 30, no. 6 (1992): 1245–68. http://dx.doi.org/10.1016/s0033-8389(22)00865-x.

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14

Lesko, E., T. Gao, R. P. Feehan, and R. Hobbs. "083 Chemically-induced cutaneous neoplasms spontaneously regress in mice lacking autoimmune regulator." Journal of Investigative Dermatology 141, no. 5 (2021): S14. http://dx.doi.org/10.1016/j.jid.2021.02.100.

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15

Yao, Ruisheng, Yian Wang, Ronald A. Lubet, and Ming You. "Differential Gene Expression in Chemically Induced Mouse Lung Adenomas." Neoplasia 5, no. 1 (2003): 41–52. http://dx.doi.org/10.1016/s1476-5586(03)80016-7.

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16

Becher, Rune, Marit Låg, Per E. Schwarze, Gunnar Brunborg, Erik J. Søderlund, and Jørn A. Holme. "Chemically induced DNA damage in isolated rabbit lung cells." Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 285, no. 2 (1993): 303–11. http://dx.doi.org/10.1016/0027-5107(93)90119-z.

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17

Huff, J. E., S. L. Eustis, and J. K. Haseman. "Occurrence and relevance of chemically induced benign neoplasms in long-term carcinogenicity studies." CANCER AND METASTASIS REVIEW 8, no. 1 (1989): 1–21. http://dx.doi.org/10.1007/bf00047055.

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18

Kamata, Tamihiro, Susan Giblett, and Catrin Pritchard. "KRASG12D expression in lung-resident myeloid cells promotes pulmonary LCH-like neoplasm sensitive to statin treatment." Blood 130, no. 4 (2017): 514–26. http://dx.doi.org/10.1182/blood-2017-02-770149.

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Key PointsKRASG12D expression in mouse lung myeloid cells induces pulmonary LCH-like neoplasms. KRASG12D-induced LCH-like neoplasms are sensitive to in vivo treatment with 3-hydroxy-3-methylglutaryl coenzyme A inhibitor atorvastatin.

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19

Kawaguchi, Akira T., Takatoshi Mizuta, Hikaru Matsuda, et al. "Single lung transplantation in rats with chemically induced pulmonary hypertension." Journal of Thoracic and Cardiovascular Surgery 103, no. 3 (1992): 483–89. http://dx.doi.org/10.1016/s0022-5223(19)34989-x.

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20

Jugg, B. J. A., A. J. Smith, S. J. Rudall, and P. Rice. "The injured lung: clinical issues and experimental models." Philosophical Transactions of the Royal Society B: Biological Sciences 366, no. 1562 (2011): 306–9. http://dx.doi.org/10.1098/rstb.2010.0235.

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Exposure of military and civilian populations to inhaled toxic chemicals can take place as a result of deliberate release (warfare, terrorism) or following accidental releases from industrial concerns or transported chemicals. Exposure to inhaled toxic chemicals can result in an acute lung injury, and in severe cases acute respiratory distress syndrome, for which there is currently no specific medical therapy, treatment remaining largely supportive. This treatment often requires intensive care facilities that may become overwhelmed in mass casualty events and may be of limited benefit in sever

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21

Koterov, A. N., L. N. Ushenkova, A. A. Wainson, D. Yu Usupzhanova, and A. Yu Bushmanov. "‘Healthy Worker Effect’ In Employees of Medical-Biological and Chemical Laboratories: Comparison with Effects in Nuclear Workers, in other Professional Contingents (Meta-Analyses), and the Role of the Radiation Factor." MEDICAL RADIOLOGY AND RADIATION SAFETY 70, no. 3 (2025): 70–82. https://doi.org/10.33266/1024-6177-2025-70-3-70-82.

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Based on a search in a supported database of sources for standardized mortality ratio (SMR; compared with the general population) for all causes and all cancer mortality for various professions and types of employment, in PubMed, the Cochrane Library, Elibrary, through Google, Google Scholar and in the reference lists of found sources, a complete/representative sample of studies of SMR all causes and SMR all cancer for personnel of biomedical, agricultural, chemical and some other research laboratories (a total of 39 sources and 3 reviews) was formed. Meta-analyses performed on the basis of th

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22

Johnsen, N. M., P. E. Schwarze, R. Wiger, et al. "SPONTANEOUSLY AND CHEMICALLY INDUCED CELL DEATH IN ISOLATED RAT LUNG CELLS." Biochemical Society Transactions 24, no. 4 (1996): 609S. http://dx.doi.org/10.1042/bst024609sb.

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23

Wang, Yian, Michael James, Weidong Wen, et al. "Chemopreventive Effects of Pioglitazone on Chemically Induced Lung Carcinogenesis in Mice." Molecular Cancer Therapeutics 9, no. 11 (2010): 3074–82. http://dx.doi.org/10.1158/1535-7163.mct-10-0510.

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24

Orita, Hajime, Jonathan Coulter, Ellen Tully, Francis P. Kuhajda, and Edward Gabrielson. "Inhibiting Fatty Acid Synthase for Chemoprevention of Chemically Induced Lung Tumors." Clinical Cancer Research 14, no. 8 (2008): 2458–64. http://dx.doi.org/10.1158/1078-0432.ccr-07-4177.

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25

Gillett, N. A., B. L. Stegelmeier, G. Kelly, P. J. Haley, and F. F. Hahn. "Expression of Epidermal Growth Factor Receptor in Plutonium-239-induced Lung Neoplasms in Dogs." Veterinary Pathology 29, no. 1 (1992): 46–52. http://dx.doi.org/10.1177/030098589202900106.

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The expression of epidermal growth factor receptor (EGF-R) was examined in canine lung tumors and in proliferative epithelial foci induced by plutonium-239 to determine if EGF-R was associated with specific neoplastic phenotypes or putative preneoplastic lesions. Seventeen (47%) of 36 canine lung tumors expressed EGF-R. Of these 17 tumors, three tumors hybridized with an erb-B RNA probe, which identified activated cell oncogenes. The expression of EGF-R was not correlated with tumor etiology, e.g., spontaneous versus radiation induced, but did correlate with specific histologic phenotypes. Nin

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26

Evert, M., R. Schneider-Stock, and F. Dombrowski. "Fatty acid synthase overexpression in insulin-induced and chemically induced preneoplastic hepatocellular foci and neoplasms of the rat liver." Pathology - Research and Practice 200, no. 4 (2004): 309. http://dx.doi.org/10.1016/s0344-0338(04)80607-1.

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27

Schoeb, T. R., E. E. McConnell, M. M. Juliana, J. K. Davis, M. K. Davidson, and J. R. Lindsey. "Mycoplasma pulmonis and Lymphoma in Bioassays in Rats." Veterinary Pathology 46, no. 5 (2009): 952–59. http://dx.doi.org/10.1354/vp.08-vp-0240-s-com.

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Lymphomas were reported to be induced in rats in bioassays of aspartame, methyl- tertiary-butyl ether (MTBE), and other chemicals conducted by a nonprofit cancer research organization. European regulatory authorities concluded that lymphomas in the aspartame study were caused by Mycoplasma pulmonis and suggested that this also was the case for the MTBE bioassay. To assess the role of M. pulmonis in these bioassays, we reviewed the tumor data for the aspartame and MTBE bioassays and, additionally, the organization's bioassay of methanol. For all 3 studies, the most frequently reported hematopoi

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28

Loginova, I. Yu, O. V. Kamenskaya, S. O. Danilenko, et al. "Radiation-induced lung injury in malignant thoracic neoplasms: current state of the problem, trends in prevention and rehabilitation." PULMONOLOGIYA 34, no. 4 (2024): 471–77. http://dx.doi.org/10.18093/0869-0189-2024-34-4-471-477.

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Radiation-induced lung injury is one of the most serious complications of radiation therapy in patients with malignant thoracic neoplasms. It results from accumulation of radiation dose in the lung tissue and can lead to development of various pathological changes in the lungs, such as fibrosis, pneumonitis and pulmonary hypertension. Post-radiation lung injury can significantly reduce the patient’s quality of life and worsen the prognosis. Aim. This literature review analyzes the causes of radiation-induced lung injury, describes the main clinical manifestations and diagnostic methods, and al

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29

Maleeff, Beverly E., Charles H. Kircher, Alison M. Badger, Timothy K. Hart, and Peter J. Bugelski. "Chemically induced accumulation of phospholipids in canine organ systems." Proceedings, annual meeting, Electron Microscopy Society of America 51 (August 1, 1993): 398–99. http://dx.doi.org/10.1017/s042482010014782x.

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Cationic amphiphilic drugs (CAD) are structurally characterized by their hydrophobic ring structure and hydrophilic side chain. Studies have shown that over 30 CADs with various pharmacological activities have the ability to induce phospholipid-like inclusions in peripheral blood cells and in organs such as lung, liver and spleen. SK&F 105685 is a novel cationic amphiphilic compound with immunomodulatory activity. It induces immune suppressor cell activity in many species. The purpose of this study was to determine if this compound induces cytoplasmic phospholipid inclusions in dogs.Hepari

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30

Duro de Oliveira, Krishna, Marcello Vannucci Tedardi, Bruno Cogliati, and Maria Lúcia Zaidan Dagli. "Higher Incidence of Lung Adenocarcinomas Induced by DMBA in Connexin 43 Heterozygous Knockout Mice." BioMed Research International 2013 (2013): 1–6. http://dx.doi.org/10.1155/2013/618475.

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Gap junctions are communicating junctions which are important for tissue homeostasis, and their disruption is involved in carcinogenic processes. This study aimed to verify the influence of deletion of one allele of the Connexin 43 gene on cancer incidence in different organs. The 7, 12-dimethylbenzanthracene (DMBA) carcinogenic model, using hebdomadary doses by gavage of 9 mg per animal, was used to induce tumors in Connexin 43 heterozygous or wild-type mice. The experiment began in the eighth week of the mice life, and all of them were euthanized when reaching inadequate physical condition,

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31

Dixon, D., and R. R. Maronpot. "Histomorphologic Features of Spontaneous and Chemically-Induced Pulmonary Neoplasms in B6C3F1 Mice and Fischer 344 Rats*1." Toxicologic Pathology 19, no. 4-1 (1991): 540–55. http://dx.doi.org/10.1177/019262339101900419.

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32

Ali, Naglaa A., Ghada H. Elsayed, Safaa H. Mohamed, et al. "Chia Seed (Salvia hispanica) Attenuates Chemically Induced Lung Carcinomas in Rats through Suppression of Proliferation and Angiogenesis." Pharmaceuticals 17, no. 9 (2024): 1129. http://dx.doi.org/10.3390/ph17091129.

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In 2022, 2.5 million cases of lung cancer were diagnosed, resulting in 1.8 million deaths. These statistics have motivated us to introduce a new natural product which is feasible in lung cancer therapies. This comprehensive study was performed to study the effects of chia seed extracts (70% ethanol and petroleum ether) on lung cancer in vitro and in vivo models. The invitro cytotoxicity activity of the chia extracts was studied in lung cancer cell lines (A549 cells). After 48 h, chia alcohol and ether extracts showed more inhibitory influence (IC50, 16.08, and 14.8 µg/mL, respectively) on A549

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33

Wang, Yian, Zhongqiu Zhang, Ying Yan, et al. "A Chemically Induced Model for Squamous Cell Carcinoma of the Lung in Mice." Cancer Research 64, no. 5 (2004): 1647–54. http://dx.doi.org/10.1158/0008-5472.can-03-3273.

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34

Johnson, G. A., M. B. Thompson, G. P. Cofer, D. Campen, and R. R. Maronpot. "Magnetic Resonance Imaging of Hepatic Neoplasms in the Rat." Veterinary Pathology 26, no. 4 (1989): 303–8. http://dx.doi.org/10.1177/030098588902600403.

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Magnetic resonance imaging (MRI) at microscopic resolution was done on a live rat that had chemically induced hepatic neoplasms. Beginning at the anterior aspect of the liver, 16 contiguous transaxial slices (each 1.25 mm thick) were produced using three-dimensional Fourier transform sequences. The rat had been treated with diethylnitrosamine (200 mg/kg) at 70 days of age, and, subsequently, received periodic implants of 17a-ethynylestradiol for 60 weeks. Carr-Purcell-Meiboom-Gill (CPMG) sequences (repetition time = 2,000 and echo time = 20, 40, 60, 80 ms) were done to give quantitative measur

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35

Chernikov, Ivan V., Yaroslav Yu Staroseletz, Irina S. Tatarnikova, et al. "siRNA-Mediated Timp1 Silencing Inhibited the Inflammatory Phenotype during Acute Lung Injury." International Journal of Molecular Sciences 24, no. 2 (2023): 1641. http://dx.doi.org/10.3390/ijms24021641.

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Acute lung injury is a complex cascade process that develops in response to various damaging factors, which can lead to acute respiratory distress syndrome. Within this study, based on bioinformatics reanalysis of available full-transcriptome data of acute lung injury induced in mice and humans by various factors, we selected a set of genes that could serve as good targets for suppressing inflammation in the lung tissue, evaluated their expression in the cells of different origins during LPS-induced inflammation, and chose the tissue inhibitor of metalloproteinase Timp1 as a promising target f

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36

Zhang, Shi-Yu, Shao-Chen Liu, Tamra Goodrow, Rebecca Morris, and Andres J. P. Klein-Szanto. "Increased expression of G1 cyclins and cyclin-dependent kinases during tumor progression of chemically induced mouse skin neoplasms." Molecular Carcinogenesis 18, no. 3 (1997): 142–52. http://dx.doi.org/10.1002/(sici)1098-2744(199703)18:3<142::aid-mc3>3.0.co;2-h.

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37

Li, Chunjie, Yian Wang, Song Gao, Ming Hu, and Ming You. "The Chemoprevention Effects of Two Herbal Mixtures on Chemically Induced Lung Tumorigenesis in Mice." Pharmaceuticals 16, no. 12 (2023): 1666. http://dx.doi.org/10.3390/ph16121666.

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Ruan Hua Tang (RHT) and Ruan Hua Fang (RHF) are two Chinese herbal mixtures that have been used in clinical cancer treatment for decades. This study validated our hypothesis that RHT and RHF can inhibit lung tumor development in the mouse model of Benzo(a)pyrene-induced lung tumorigenesis. An RHT oral solution was diluted to 9% and 18% in water. RHF was mixed into the diet at 15% and 30% of total food in the final doses. Two weeks after injecting BP into mice, we administered RHT and RHF for eighteen weeks. We found that 9% and 18% RHT reduced tumor multiplicity by 36.05% and 38.81% (both p &l

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38

Takahashi, Kota, Satoru Ito, Kishio Furuya, Shuichi Asano, Masahiro Sokabe, and Yoshinori Hasegawa. "Real-time imaging of mechanically and chemically induced ATP release in human lung fibroblasts." Respiratory Physiology & Neurobiology 242 (August 2017): 96–101. http://dx.doi.org/10.1016/j.resp.2017.04.008.

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39

Zanaboni, P. B., J. D. Bradley, L. J. Baudendistel, R. O. Webster, and T. E. Dahms. "Cyclooxygenase inhibition prevents PMA-induced increases in lung vascular permeability." Journal of Applied Physiology 69, no. 4 (1990): 1494–501. http://dx.doi.org/10.1152/jappl.1990.69.4.1494.

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The effect of cyclooxygenase inhibition in phorbol myristate acetate (PMA)-induced acute lung injury was studied in isolated constant-flow blood-perfused rabbit lungs. PMA caused a 51% increase in pulmonary arterial pressure (localized in the arterial and middle segments as measured by vascular occlusion pressures), a 71% increase in microvascular permeability (measured by the microvascular fluid filtration coefficient, Kf), and a nearly threefold increase in perfusate thromboxane (Tx) B2 levels. Cyclooxygenase inhibition with three chemically dissimilar inhibitors, indomethacin (10(-7) and 10

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40

Solopov, Pavel, Ruben Manuel Luciano Colunga Biancatelli, Christiana Dimitropoulou, and John D. Catravas. "Dietary Phytoestrogens Ameliorate Hydrochloric Acid-Induced Chronic Lung Injury and Pulmonary Fibrosis in Mice." Nutrients 13, no. 10 (2021): 3599. http://dx.doi.org/10.3390/nu13103599.

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We previously reported that female mice exhibit protection against chemically induced pulmonary fibrosis and suggested a potential role of estrogen. Phytoestrogens act, at least in part, via stimulation of estrogen receptors; furthermore, compared to residents of Western countries, residents of East Asian countries consume higher amounts of phytoestrogens and exhibit lower rates of pulmonary fibrosis. Therefore, we tested the hypothesis that dietary phytoestrogens ameliorate the severity of experimentally induced pulmonary fibrosis. Male mice placed on either regular soybean diet or phytoestro

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41

O'Brien, K. A. F., L. L. Smith, and G. M. Cohen. "Inability of a human lung tumour cell line (A549) to detect chemically induced organ-specific toxicity to the lung." Toxicology in Vitro 1, no. 2 (1987): 85–90. http://dx.doi.org/10.1016/0887-2333(87)90005-1.

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42

Solopov, Pavel, Ruben Manuel Luciano Colunga Biancatelli, Christiana Dimitropoulou, and John D. Catravas. "Sex-Related Differences in Murine Models of Chemically Induced Pulmonary Fibrosis." International Journal of Molecular Sciences 22, no. 11 (2021): 5909. http://dx.doi.org/10.3390/ijms22115909.

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We developed two models of chemically induced chronic lung injury and pulmonary fibrosis in mice (intratracheally administered hydrochloric acid (HCl) and intratracheally administered nitrogen mustard (NM)) and investigated male–female differences. Female mice exhibited higher 30-day survival and less weight loss than male mice. Thirty days after the instillation of either HCl or NM, bronchoalveolar lavage fluid displayed a persistent, mild inflammatory response, but with higher white blood cell numbers and total protein content in males vs. females. Furthermore, females exhibited less collage

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43

Herbert, R. A., B. S. Stegelmeier, N. A. Gillett, et al. "Plutonium-induced Proliferative Lesions and Pulmonary Epithelial Neoplasms in the Rat: Immunohistochemical and Ultrastructural Evidence for Their Origin from Type II Pneumocytes." Veterinary Pathology 31, no. 3 (1994): 366–74. http://dx.doi.org/10.1177/030098589403100310.

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Immunohistochemistry and transmission electron microscopy were used to clarify the cellular origin for plutonium-239-induced pulmonary proliferative (preneoplastic) epithelial lesions and epithelial neoplasms in F344 rats. Examples of each histologic type of proliferative lesion and neoplasm were stained by the avidin-biotin complex immunoperoxidase method using antibodies to rat surfactant apoprotein and Clara cell antigen. Rat surfactant apoprotein immunostaining was detected in type II pneumocytes in sections of normal lung, in the cells of the proliferative lesions classified histologicall

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44

Taras, Danièle, Jean-Frédéric Blanc, Anne Rullier, et al. "Halofuginone suppresses the lung metastasis of chemically induced hepatocellular carcinoma in rats through MMP inhibition." Neoplasia 8, no. 4 (2006): 312–18. http://dx.doi.org/10.1593/neo.05796.

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45

NAKAYAMA, Tsutomu, Itsuko HARAGUCHI, Kei HASHIMOTO, Yasunori SUGIYAMA, and Toshihiko OSAWA. "Suppression of Hydrogen Peroxide-Induced Cytotoxicity toward Chinese Hamster Lung Fibroblasts by Chemically Modified Curcumin." Food Science and Technology International, Tokyo 3, no. 1 (1997): 74–76. http://dx.doi.org/10.3136/fsti9596t9798.3.74.

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Zhang, Xiaoying, Wenjing Tang, Haoyu Wen, et al. "Evaluation of CTB-sLip for Targeting Lung Metastasis of Colorectal Cancer." Pharmaceutics 14, no. 4 (2022): 868. http://dx.doi.org/10.3390/pharmaceutics14040868.

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Lung metastasis of colorectal cancer is common in the clinic; however, precise targeting for the diagnosis and therapy purposes of those lung metastases remains challenging. Herein, cholera toxin subunit b (CTB) protein was chemically conjugated on the surface of PEGylated liposomes (CTB-sLip). Both human-derived colorectal cancer cell lines, HCT116 and HT-29, demonstrated high binding affinity and cellular uptake with CTB-sLip. In vivo, CTB-sLip exhibited elevated targeting capability to the lung metastasis of colorectal cancer in the model nude mice in comparison to PEGylated liposomes (sLip

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Barabutis, Nektarios, Christiana Dimitropoulou, Charalampos Birmpas, Atul Joshi, Gagan Thangjam, and John D. Catravas. "p53 protects against LPS-induced lung endothelial barrier dysfunction." American Journal of Physiology-Lung Cellular and Molecular Physiology 308, no. 8 (2015): L776—L787. http://dx.doi.org/10.1152/ajplung.00334.2014.

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New therapies toward heart and blood vessel disorders may emerge from the development of Hsp90 inhibitors. Several independent studies suggest potent anti-inflammatory activities of those agents in human tissues. The molecular mechanisms responsible for their protective effects in the vasculature remain unclear. The present study demonstrates that the transcription factor p53, an Hsp90 client protein, is crucial for the maintenance of vascular integrity, protects again LPS-induced endothelial barrier dysfunction, and is involved in the mediation of the anti-inflammatory activity of Hsp90 inhib

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Zanaboni, P. B., J. D. Bradley, R. O. Webster, and T. E. Dahms. "Cyclooxygenase inhibitors prevent ethchlorvynol-induced injury in rat and rabbit lungs." Journal of Applied Physiology 71, no. 1 (1991): 43–49. http://dx.doi.org/10.1152/jappl.1991.71.1.43.

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The effect of three chemically dissimilar cyclooxygenase inhibitors on ethchlorvynol-(ECV) induced acute lung injury was studied in isolated buffer-perfused rat and blood-perfused rabbit lungs. ECV caused the microvascular fluid filtration coefficient (Kf) to increase by greater than threefold in the rat lungs and twofold in the rabbit lungs. ECV caused increased pulmonary vascular resistance (PVR) and microvascular pressure measured by the double occlusion technique (Pdo) compared with the vehicle control group in the rat experiments. However, ECV had no effect on PVR or Pdo in the rabbit exp

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Fathalla, A. S., M. A. Ibrahim, S. R. Mohamed, et al. "Histological and ultrastructural studies on the effect of Cassia alata methanolic leaf extracts against chemically induced lung adenocarcinoma in rats." Arquivo Brasileiro de Medicina Veterinária e Zootecnia 75, no. 5 (2023): 857–71. http://dx.doi.org/10.1590/1678-4162-13047.

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ABSTRACT The present work aims to evaluate anticancer performance of Cassia alata methanolic leaf extracts (CMLE) in ethyl carbamate-stimulated lung adenocarcinoma (LAD) in differentiation to the function of Cisplatin (CIPL). Rats were divided into four groups: (1) control (CONT), (2) lung-adenocarcinoma (LAD) injected intra-peritoneally with 1g/kg ethyl carbamate once weekly for a month, (3) LAD+CMLE administered 500 mg/kg CMLE orally for the last two months of the experiment, and (4) LAD+CIPL treated group, injected 2.5 mg/kg Cisplatin intraperitoneally once weekly for the last two months of

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Balakrishna, Shrilatha, Weifeng Song, Satyanarayana Achanta, et al. "TRPV4 inhibition counteracts edema and inflammation and improves pulmonary function and oxygen saturation in chemically induced acute lung injury." American Journal of Physiology-Lung Cellular and Molecular Physiology 307, no. 2 (2014): L158—L172. http://dx.doi.org/10.1152/ajplung.00065.2014.

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The treatment of acute lung injury caused by exposure to reactive chemicals remains challenging because of the lack of mechanism-based therapeutic approaches. Recent studies have shown that transient receptor potential vanilloid 4 (TRPV4), an ion channel expressed in pulmonary tissues, is a crucial mediator of pressure-induced damage associated with ventilator-induced lung injury, heart failure, and infarction. Here, we examined the effects of two novel TRPV4 inhibitors in mice exposed to hydrochloric acid, mimicking acid exposure and acid aspiration injury, and to chlorine gas, a severe chemi

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