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Alterations in Apoptotic Cell Populations, Protein Markers, and Gene Expression Patterns in Rats with Sulfur
1Department of Respiration, The 80th Group Army Hospital of People's Liberation Army, Weifang, China. LTT2008L@163.com.
Iranian Journal of Allergy, Asthma, and Immunology
|May 11, 2026
Summary
Sulfur mustard (SM) exposure causes lung injury via apoptosis. Intraperitoneal SM injection induced more severe apoptotic responses in lung cells than intratracheal instillation, identifying potential therapeutic targets.
Area of Science:
- Toxicology
- Cellular Biology
- Pulmonary Medicine
Background:
- Sulfur mustard (SM) is a chemical warfare agent causing severe injuries, particularly life-threatening respiratory damage.
- The precise cellular mechanisms of SM-induced apoptosis in the lungs are not fully understood.
- Identifying these mechanisms is crucial for developing effective countermeasures.
Purpose of the Study:
- To investigate the apoptotic pathways activated by SM in the lung.
- To compare the severity of SM-induced apoptosis via different exposure routes (intraperitoneal vs. intratracheal).
- To identify potential molecular targets for therapeutic intervention.
Main Methods:
- Induction of acute lung injury in a rat model using intraperitoneal injection and intratracheal instillation of SM (1 LD50 dose).
- Assessment of apoptosis using TUNEL staining, immunohistochemistry, and quantitative real-time PCR.
- Analysis of apoptosis-related proteins and gene expression, including annexin A1, annexin A2, cytochrome C, caspase-12, and JNK3.
Main Results:
- Intraperitoneal SM administration significantly elevated apoptotic markers (annexin A1, annexin A2, cytochrome C, caspase-12, JNK3) in alveolar epithelial cells.
- These increases were more pronounced compared to intratracheal SM instillation at equivalent doses.
- TUNEL assays and immunohistochemistry confirmed heightened apoptosis with intraperitoneal exposure.
Conclusions:
- Intraperitoneal exposure to sulfur mustard triggers a more severe apoptotic response in alveolar epithelial cells than intratracheal exposure.
- The intraperitoneal model effectively identifies apoptosis-related molecular targets for potential therapeutic development against SM-induced lung injury.
