Objective: To investigate the oxidative damage to lung tissue and peripherial blood in PM2.5-treated rats.
Methods: PM2.5 samples were collected using an auto-sampling instrument in summer and winter. Treated samples were endotracheally instilled into rats. Activity of reduced glutathione peroxidase (GSH-Px) and concentration of malondialdehyde (MDA) were used as oxidative damage biomarkers of lung tissue and peripheral blood detected with the biochemical method. DNA migration length (microm) and rate of tail were used as DNA damage biomarkers of lung tissue and peripheral blood detected with the biochemical method.
Results: The activity of GSH-Px and the concentration of MDA in lung tissue significantly decreased after exposure to PM2.5 for 7-14 days. In peripheral blood, the concentration of MDA decreased, but the activity of GSH-Px increased 7 and 14 days after experiments. The two indicators had a dose-effect relation and similar changing tendency in lung tissue and peripheral blood. The DNA migration length (microm) and rate of tail in lung tissue and peripheral blood significantly increased 7 and 14 days after exposure to PM2.5. The two indicators had a dose-effect relation and similar changing tendency in lung tissue and peripheral blood.
Conclusion: PM2.5 has a definite oxidative effect on lung tissue and peripheral blood. The activity of GSH-Px and the concentration of MDA are valuable biomarkers of oxidative lung tissue damage induced by PM2.5. The DNA migration length (microm) and rate of tail are simple and valuable biomarkers of PM2.5-induced DNA damage in lung tissues and peripheral blood. The degree of DNA damage in peripheral blood can predict the degree of DNA damage in lung tissue.
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http://dx.doi.org/10.1016/S0895-3988(09)60049-0 | DOI Listing |
J Infect Dev Ctries
December 2024
Department of Pulmonary and Respiratory Medicine, Faculty of Medicine, Universitas Airlangga, Surabaya, Indonesia.
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Int J Biol Macromol
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Department of Oncology, the Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, PR China; Nuclear Medicine and Molecular Imaging Key Laboratory of Sichuan Province, Luzhou, Sichuan 646000, PR China. Electronic address:
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January 2025
Bielefeld University, Medical School and University Medical Center OWL, Lung Cancer Center Lippe, Department of Pathology, Klinikum Lippe Detmold, 32756 Detmold, Germany. Electronic address:
Intraoperative consultation is frequently used during the surgical treatment of lung tumors for the diagnosis of malignancy and the assessment of surgical margins. The latter is often problematic given the nature of the applied staple lines, which cannot be readily examined in frozen sections. Seventy-nine samples of surgical margins (71 staple lines and 8 open margins) from 52 lung specimens were examined using an ex vivo fluorescence confocal microscope (FCM).
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Key Laboratory of Medicine, Ministry of Education, School of Laboratory Medicine and Life Sciences, Wenzhou Medical University; Wenzhou, Zhejiang 325035, China; Oujiang Laboratory (Zhejiang Lab for Regenerative Medicine, Vision and Brain Health), Wenzhou, Zhejiang 325053, China. Electronic address:
Cigarette smoking (CS) is one of the greatest health concerns, which can cause lung cancer. 4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), a tobacco-specific nitrosamine, and has been well-documented for its carcinogenic activity in both epidemiological and laboratory studies. PH domain leucine-rich repeat protein phosphatase 1 (PHLPP1) and phosphatase and tensin homolog (PTEN) are two well-known phosphatase tumor suppressors that have been reported to be downregulated in human lung cancer tissues.
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University of Colorado, Anschutz Medical Campus School of Medicine| Translational research laboratory of Red Blood Cell Diseases and Hypoxia related illnesses| Cardiovascular Pulmonary Research (CVP) group, Pediatrics. Electronic address:
Lung tissue from human patients and murine models of sickle cell disease pulmonary hypertension (SCD-PH) show perivascular regions with excessive iron accumulation. The iron accumulation arises from chronic hemolysis and extravasation of hemoglobin (Hb) into the lung adventitial spaces, where it is linked to nitric oxide depletion, oxidative stress, inflammation, and tissue hypoxia, which collectively drive SCD-PH. Here, we tested the hypothesis that intrapulmonary delivery of hemopexin (Hpx) to the deep lung is effective at scavenging heme-iron and attenuating the progression of SCD-PH.
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