Abstract
Rationale: Many studies report that respiratory diseases are associated with increased free radicals (FR) production. AAPH is a FR-generating compound. Aim: To investigate whether AAPH is able to impair lung function, histology and biochemical processes. Methods: This study was approved by the Ethics Committee on Animal Use under code IBCCF128. Male Wistar rats received one intranasal instillation of saline solution (714 μL/kg, n=8) or different amounts of AAPH (25, 50, 100 or 200 mg/kg in saline solution, 714 μL/kg, n=38). 72 h after the instillation pulmonary mechanics was determined, lungs were prepared for histology and lung homogenates were biochemically assayed for antioxidant status. One-way ANOVA followed by Holm-Sidak test was used (α= 5%). Results: Central airway resistive pressure was higher in AAPH100 and AAPH200 (0.74±0.25 and 0.92±0.45 cmH2O, respectively) than in SS (0.38±0.12 cmH2O). Static elastance was larger in AAPH200 (2.72±0.61 cmH2O/mL) than in SS (2.10±0.31 cmH2O/mL). Superoxide dismutase activity in AAPH200 (2.45±0.49 U/mg protein) was smaller than in SS (5.21±1.02 U/mg protein). Catalase activity in AAPH200 (17.32±3.69 U/mg protein) was higher than in SS (7.63±1.58 U/mg protein). Levels of carbonyl groups in AAPH100 and AAPH200 (0.85±0.41 and 1±0.18 U/mg protein, respectively) were higher than in SS (0.39±0.11 U/mg protein). The bronchoconstriction indexes in AAPH25, AAPH50, AAPH100 and AAPH200 (4.15±0.38, 4.20±0.46, 4.28±0.46 and 4.15±0.55, respectively) were higher than in SS (3.23±0.19). Conclusion: AAPH impairs pulmonary mechanics and morphology and induces oxidant-antioxidant imbalance. Supported by: CNPq, FAPERJ, FUNCAP, CAPES.
- © 2014 ERS
