Related Experiment Videos
Effect of oxygen concentration on pulmonary fibrosis caused by peplomycin in mice
Abstract:
The pulmonary fibrosis caused by peplomycin (PEP) was studied in terms of oxygen toxicity using ICR mice. When 16 micrograms of PEP was administered intratracheally in mice after exposure to the air containing 75% O2 for 10 days, the pulmonary fibrosis was completely suppressed, while when mice were exposed to 75% O2 after the administration of PEP, the fibrosis was much severe than that of mice raised in atmospheric air. In 50% O2, similar oxygen effect was also observed, but it was weaker than that in 75% O2. In 90% O2, the oxygen toxicity was observed in mice without administration of PEP. When mice were exposed to 75% O2, the activities of superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase, which are relevant to the detoxication of active oxygen species, were not increased in the lung, but the levels of reducing agents such as glutathione and ascorbic acid, and high molecular substances having 1O2-scavenging activity were enhanced. The results suggest that these materials have some roles to decrease the pulmonary fibrosis caused by PEP.
Insights
Peplomycin-induced pulmonary fibrosis is suppressed when mice breathe 75% oxygen after treatment. However, fibrosis worsens if oxygen exposure precedes peplomycin administration, indicating oxygen
Area of Science:
- Pulmonary Medicine
- Toxicology
- Biochemistry
Background:
- Pulmonary fibrosis is a debilitating lung disease.
- Peplomycin (PEP) is a chemotherapeutic agent known to induce pulmonary fibrosis.
- Oxygen toxicity plays a complex role in lung injury.
Purpose of the Study:
- To investigate the influence of oxygen toxicity on peplomycin-induced pulmonary fibrosis in mice.
- To elucidate the mechanisms underlying the interaction between oxygen exposure and PEP-induced lung damage.
Main Methods:
- ICR mice were used to model pulmonary fibrosis.
- Mice received intratracheal administration of peplomycin (16 micrograms).
- Mice were exposed to varying concentrations of oxygen (50%, 75%, 90%) at different time points relative to PEP administration.
Main Results:
- Pulmonary fibrosis was completely suppressed when PEP was administered after 10 days of exposure to 75% oxygen.
- Fibrosis was significantly exacerbated when mice were exposed to 75% oxygen after PEP administration.
- In 50% oxygen, a similar but weaker effect was observed; 90% oxygen induced toxicity without PEP.
- Enzymatic antioxidant activities (SOD, catalase, GPx, GR) in the lung did not increase with 75% oxygen exposure.
- Levels of reducing agents (glutathione, ascorbic acid) and 1O2-scavenging substances increased in the lung under 75% oxygen.
Conclusions:
- The timing of oxygen exposure relative to peplomycin administration critically affects pulmonary fibrosis severity.
- Enhanced levels of reducing agents and 1O2-scavenging substances in the lung may contribute to the suppression of PEP-induced fibrosis under specific oxygen conditions.