Related Experiment Video
Updated: Oct 13, 2025
Oropharyngeal Administration of Bleomycin in the Murine Model of Pulmonary Fibrosis
Published on: May 9, 2025
Atrazine Inhalation Worsen Pulmonary Fibrosis Regulating the Nuclear Factor-Erythroid 2-Related Factor (Nrf2)
Ramona D'Amico1, Francesco Monaco2, Roberta Fusco1
1Department of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, Messina, Italy.
Background/Aims:
Pulmonary fibrosis can be caused by genetic abnormalities, autoimmune disorders or exposure to environmental pollutants. All these causes have in common the excessive production of oxidative stress species that initiate a cascade of molecular mechanism underlying fibrosis in a variety of organs, including lungs. The chemical name of Atrazine (ATR) is 6-chloro-N-ethyl-N'-(1-methylethyl)-1,3,5-triazine-2,4-diamine, and it is the most commonly used broad-spectrum herbicide in agricultural crops. Additionally, Bleomycin is a chemotherapeutic agent often used for different lymphoma with a seriously pulmonary complication. The most accredited hypothesis that may explain the mechanism of toxicity induced by ATR or bleomycin is exactly the production of reactive oxygen species (ROS) that leads to an unbalance in the physiological anti-oxidant system. However, until today, nobody has investigated the effect of ATR exposure during pulmonary fibrosis.
Methods:
Mice were subject to ATR exposure, to bleomycin injection or to both. At the end of experiment, the lungs and blood were collected. Additionally, we analyzed by different test such as open field, pole and rotarod test or other we investigated the effects of ATR or bleomycin exposure on behavior.
Results:
Following ATR or bleomycin induction, we found a significant increase in lung damage, fibrosis, and oxidative stress. This condition was significantly worsened when the animals injected with bleomycin were also exposed to ATR. Additionally, we observed significant motor and non-motor impairment in animals exposed to ATR.
Conclusion:
Our study demonstrates that ATR exposure, decrease nuclear factor-erythroid 2-related factor (Nrf2) pathways in both lung and brain.
Insights
Atrazine (ATR) exposure worsens lung fibrosis and oxidative stress, particularly when combined with bleomycin. This herbicide also impairs motor function and decreases protective Nrf2 pathways in the lungs and brain.
Area of Science:
- Environmental toxicology
- Pulmonary medicine
- Neuroscience
Background:
- Pulmonary fibrosis stems from oxidative stress, common in genetic, autoimmune, or environmental causes.
- Atrazine (ATR), a widely used herbicide, and bleomycin, a chemotherapy drug, induce oxidative stress.
- The impact of ATR on pulmonary fibrosis remains uninvestigated.
Purpose of the Study:
- To investigate the effects of Atrazine (ATR) exposure on pulmonary fibrosis.
- To determine if ATR exacerbates bleomycin-induced lung injury.
- To assess the impact of ATR on oxidative stress and Nrf2 pathways.
Main Methods:
- Mice were exposed to ATR, bleomycin, or both.
- Lung and blood samples were collected for analysis.
- Behavioral tests (open field, rotarod) assessed motor function.
Main Results:
- ATR and bleomycin significantly increased lung damage, fibrosis, and oxidative stress.
- Combined ATR and bleomycin exposure worsened lung pathology.
- ATR exposure led to significant motor and non-motor impairments.
Conclusions:
- ATR exposure exacerbates pulmonary fibrosis and oxidative stress.
- ATR negatively impacts neurological function.
- ATR exposure downregulates the protective Nrf2 pathway in the lungs and brain.
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