Acute exposure to nitrogen mustard induces rapid nuclear component regulation and delayed stress to exogenous stimuli.

Nitrogen mustard (NM) is a vesicant agent with potent toxic effects on various tissues. Numerous theories have been proposed to explain its toxic mechanisms, yet research on the interconnections among these theories is lacking. This study focuses on analyzing the characteristics of genes involved in NM-induced bronchial injury within the Comparative Toxicogenomics Database (CTD). Subsequently, based on the CTD, we compared and analyzed the acute exposure and delayed changes following exposure in 16HBE cells. The injury processes caused by NM to bronchial and skin tissues are similar, primarily involving metabolism and regulation of nuclear constituents and inflammatory responses within the cellular matrix. During the acute exposure phase, NM rapidly induces nuclear stress, with the JUN family at the core of regulating metabolic and nucleic acid activities, and various nuclear binding proteins exhibit abnormalities. Delayed reactions following acute exposure are primarily centered in the cytoplasmic region, with diverse reaction types, including oxidative stress and responses to exogenous stimuli. Abnormalities in the activity of multiple cellular matrix enzymes are observed, with a relatively even involvement of various stress responses. Communication between the nucleus and cytoplasm is extreme active during the injury, and the content of the communication changes over time. These results suggest a temporal sequence in which NM causes chromatin damage and mediates cytoplasmic stress responses. In prevention and first aid, rapid DNA repair should be the primary focus, while subsequent treatment after acute exposure should focus more on delayed inflammatory and oxidative stress responses.