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The study establishes the efficacy of NAC in mitigating some effects of Cl₂-induced lung damage but notes limited success in addressing AHR. Could the authors elaborate on why the timing and dosing regimens for NAC and NACA were not optimized for AHR mitigation? Given the similar outcomes between NAC and NACA, how might these findings influence the practical or clinical adoption of the more costly amide derivative?
Since neither NAC nor NACA significantly alleviated AHR, could alternative inflammatory or neuromodulatory pathways be contributing to persistent airway dysfunction? Additionally, the ex vivo pig lung slice model is a valuable translational tool, but were any functional differences observed between mouse and pig lung responses to NAC/NACA treatment?