ArticleHistochemistry and cell biology2006
In situ assessment of oxidant and nitrogenic stress in bleomycin pulmonary fibrosis.
Article in Histochemistry and cell biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
23 citing papers in PubMed, 50 citations in OpenAlex.
- SS-31: A promising therapeutic agent against bleomycin-induced pulmonary fibrosis in Mice.PloS one · 2025Article
- Nintedanib Ameliorates Bleomycin-Induced Pulmonary Fibrosis, Inflammation, Apoptosis, and Oxidative Stress by Modulating PI3K/Akt/mTOR Pathway in Mice.Inflammation · 2023Article
- Inhibition of Fatty Acid Amide Hydrolase (FAAH) Regulates NF-kb Pathways Reducing Bleomycin-Induced Chronic Lung Inflammation and Pulmonary Fibrosis.International journal of molecular sciences · 2023Article
- Baicalin alleviates bleomycin‑induced pulmonary fibrosis and fibroblast proliferation in rats via the PI3K/AKT signaling pathway.Molecular medicine reports · 2020Article
- A Potential Link Between Oxidative Stress and Endothelial-to-Mesenchymal Transition in Systemic Sclerosis.Frontiers in immunology · 2018Review
- Region-specific role for Pten in maintenance of epithelial phenotype and integrity.American journal of physiology. Lung cellular and molecular physiology · 2017Article
- Mitochondrial catalase overexpressed transgenic mice are protected against lung fibrosis in part via preventing alveolar epithelial cell mitochondrial DNA damage.Free radical biology & medicine · 2016Article
- Abnormal B lymphocyte activation and function in systemic sclerosis.Annals of dermatology · 2015Review
- Protective effect of dexpanthenol on bleomycin-induced pulmonary fibrosis in rats.Naunyn-Schmiedeberg's archives of pharmacology · 2013Article
- Pulmonary toxicity and fibrogenic response of carbon nanotubes.Toxicology mechanisms and methods · 2013Review
- Reactive oxygen species-mediated p38 MAPK regulates carbon nanotube-induced fibrogenic and angiogenic responses.Nanotoxicology · 2013Article
- Early alveolar epithelial dysfunction promotes lung inflammation in a mouse model of Hermansky-Pudlak syndrome.American journal of respiratory and critical care medicine · 2011Article
- Lung extracellular superoxide dismutase overexpression lessens bleomycin-induced pulmonary hypertension and vascular remodeling.American journal of respiratory cell and molecular biology · 2011Article
- Macrophages and tissue injury: agents of defense or destruction?Annual review of pharmacology and toxicology · 2011Review
- Macrophages, reactive nitrogen species, and lung injury.Annals of the New York Academy of Sciences · 2010Review
- Phosphatidylinositol-3-kinase/akt regulates bleomycin-induced fibroblast proliferation and collagen production.American journal of respiratory cell and molecular biology · 2010Article
- Clinical significance of serum HMGB-1 and sRAGE levels in systemic sclerosis: association with disease severity.Journal of clinical immunology · 2009Article
- Anti-oxidant inhibition of hyaluronan fragment-induced inflammatory gene expression.Journal of inflammation (London, England) · 2008Article
- Oxidative stress, plasminogen activator inhibitor 1, and lung fibrosis.Antioxidants & redox signaling · 2008Review
- Antioxidants as potential therapeutics for lung fibrosis.Antioxidants & redox signaling · 2008Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reactive oxygen species (ROS) and nitric oxide (NO) have a role in the development of pulmonary fibrosis after bleomycin administration. The ROS production induces an antioxidant response, involving superoxide dismutases (SODs), catalase, and glutathione peroxidases. We compared in situ oxidative burden and antioxidant enzyme activity in bleomycin-injured rat lungs and normal controls. ROS expression and catalase, glucose-6-phosphate-dehydrogenase (G6PHD), and NOS/NADPH-diaphorase activity were investigated by using histochemical reactions. Nitric oxide synthase (e-NOS and i-NOS) and SOD (MnSOD, Cu/ZnSOD, ECSOD) expression was investigated immunohistochemically. After treatment ROS production was enhanced in both phagocytes and in type II alveolar epithelial cells. Mn, Cu/Zn, and ECSOD were overexpressed in parenchymal cells, whereas interstitium expressed ECSOD. Catalase and G6PHD activity was moderately increased in parenchymal and inflammatory cells. NOS/NADPH-d activity and i-NOS expression increased in alveolar and bronchiolar epithelia and in inflammatory cells. It can be suggested that the concomitant activation of antioxidant enzymes is not adequate to scavenge the oxidant burden induced by bleomycin lung damage. Inflammatory cells and also epithelial cells are responsible of ROS and NO production. This oxidative and nitrosative stress may be a substantial trigger in TGF-beta1 overexpression by activated type II pneumocytes, leading to fibrotic lesions.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.