Bleomycin
Bleomycin - Related Videos
06:03
Oropharyngeal Administration of Bleomycin in the Murine Model of Pulmonary Fibrosis
0 Views •
Cited by 2 •
2025
This protocol demonstrates the oropharyngeal aspiration technique for use in the bleomycin murine model of pulmonary fibrosis.
02:46
A Mouse Model of Pulmonary Fibrosis Induced by Nasal Bleomycin Nebulization
0 Views •
Cited by 4 •
2023
Various animal models of pulmonary fibrosis have been established using bleomycin to clarify the pathogenesis of pulmonary fibrosis and find new drug targets. However, most pulmonary fibrosis models targeting lung tissue have uneven drug administration. Here, we propose a model of uniform pulmonary fibrosis induced by nasal bleomycin nebulization.
05:45
A Refined Aerosol-Based Intratracheal Bleomycin Delivery Method for Reproducible and Minimally Invasive Mouse Models of Pulmonary Fibrosis
0 Views •
2026
Here, we present a protocol to model pulmonary fibrosis in mice using aerosolized bleomycin delivered via the trachea. This optimized method enables uniform, quantitative, and precise delivery without surgical incision, enhancing the reproducibility and reliability of bleomycin-induced fibrosis.
06:29
Adoptive Transfer of IL-33-Stimulated Macrophages into Bleomycin-Induced Mouse Models to Study Their Effect on Idiopathic Pulmonary Fibrosis In Vivo
0 Views •
Cited by 1 •
2023
This protocol describes the isolation of pulmonary interstitial macrophages (IMs) and their adoptive transfer after IL-33 stimulation of the lung alveoli in a mouse model, which can facilitate the in vivo study of idiopathic pulmonary fibrosis (IPF).
06:52
Induction of Mouse Lung Injury by Endotracheal Injection of Bleomycin
0 Views •
Cited by 13 •
2019
Here we present an effective method to investigate the antifibrotic activity of intravenously infused human mesenchymal stromal cells obtained from the whole umbilical cord following the induction of lung injury by an endotracheal injection of bleomycin in C57BL/6 mice. This protocol can be easily extended to the preclinical testing of other therapeutics.
FAQs
Bleomycin’s DNA-damaging activity follows a coordinated sequence: the drug first associates with DNA, then its iron-coordinating complex reacts in the presence of oxygen. This chemistry generates reactive radicals capable of cleaving DNA strands. The resulting lesions can interfere with replication, linking a molecular reaction to broader cellular stress and explaining its value in cancer biology research.
Both iron and oxygen are essential conditions for the radical-generating step. Iron provides the coordinated center of the bleomycin complex, while oxygen enables formation of the reactive species that attack DNA. Without this sequence, DNA strand cleavage would not follow the same mechanism. This dependence helps researchers connect chemical conditions with biological damage.
Cleaved DNA can disrupt replication, so the initial molecular injury may become a broader cellular stress response. This relationship is important when interpreting experimental systems: researchers can use bleomycin exposure to investigate how cells respond to DNA damage, rather than examining DNA breakage as an isolated chemical event.
In clinical oncology, bleomycin is used with other agents for selected cancers rather than presented as a standalone treatment in the supplied context. The overview specifically identifies lymphomas and germ-cell tumors as examples. Its inclusion also requires attention to dose-limiting lung toxicity, which is a major biological constraint on treatment.
Researchers apply bleomycin in laboratory models to examine DNA damage, cellular stress, and tissue injury, including pulmonary fibrosis. These models let investigators connect the drug’s molecular effects with changes in tissue biology. The same experimental context is therefore relevant to both basic mechanisms and the study of lung-related toxicity.
Its effects span different biological levels: DNA strand cleavage can disrupt replication in cancer-related studies, while injury to pulmonary tissue underlies its dose-limiting toxicity and motivates fibrosis models. Studying both contexts helps biology researchers compare a drug’s intended anticancer role with harmful tissue consequences.