ANTIOXIDANT ENZYME ACTIVITIES

Salbutamol, montelukast, and prednisolone are commonly prescribed for respiratory disorders. While their therapeutic effects on the airways are well documented, their impact on pulmonary oxidative stress and antioxidant defense mechanisms remains less understood. This study investigated the effects of these drugs and their combinations on oxidative stress biomarkers and total protein concentration in lung tissue. Experimental animals were assigned to eight groups (n = 4): negative control, positive control, salbutamol, montelukast, prednisolone, salbutamol/prednisolone, salbutamol/montelukast, and prednisolone/montelukast. Lung tissue homogenates were analyzed for total protein concentration, antioxidant enzyme activitiesincluding superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx)-and oxidative markers, specifically hydrogen peroxide (H2O2) and nitric oxide (NO). Data were expressed as mean ±SEM and analyzed by one-way ANOVA with significance set at p < 0.05. Total protein concentration and catalase activity were not significantly altered in any treatment group compared with the negative control (p > 0.05). Prednisolone treatment significantly increased SOD activity relative to the negative control (p < 0.05), whereas GPx activity was elevated only in the positive control group. Montelukast significantly increased H202 levels compared with the negative control, but H202 levels in the salbutamol, montelukast, and prednisolone groups were significantly lower than the positive control. Nitric oxide concentration decreased in the positive control and prednisolone groups relative to the negative control, while montelukast treatment caused a significant increase in NO compared with the positive control (p < 0.05).

Salbutamol, montelukast, and prednisolone are widely used in the management of respiratory disorders. Despite their therapeutic benefits, their effects on pulmonary oxidative stress and antioxidant defenses, particularly when used in combination, remain unclear. This study evaluated the influence of these agents on oxidative stress markers and total protein concentration in lung tissue. Experimental animals were divided into five groups (n = 8 group): negative control, positive control, salbutamol, montelukast, prednisolone, salbutamol/prednisolone, salbutamol/montelukast, and prednisolone/montelukast. Lung tissue homogenates were analyzed for total protein concentration, antioxidant enzyme activities superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx)—and oxidative stress markers, including hydrogen peroxide (H₂O₂) and nitric oxide (NO). Data were expressed as mean ± SEM and analyzed using one-way ANOVA with significance set at p < 0.05. Total protein concentration significantly increased only in the salbutamol/prednisolone-treated group compared with the negative control (p < 0.05). This group also exhibited significant decreases in SOD, CAT, and GPx activities relative to both negative and positive controls (p < 0.05), indicating reduced antioxidant capacity. In contrast, salbutamol/montelukast and prednisolone/montelukast treatments did not alter protein concentration or most antioxidant enzymes compared with the negative control, although CAT and GPx were decreased relative to the positive control (p < 0.05). Hydrogen peroxide levels were significantly elevated in salbutamol/montelukast and prednisolone/montelukast groups compared with the negative
control (p < 0.05), while NO levels did not differ significantly among groups. However, compared with the positive control, NO concentration increased in salbutamol/prednisolone and salbutamol/montelukast groups (p < 0.05). In conclusion, combination therapy with salbutamol and prednisolone reduces pulmonary antioxidant enzyme activity while increasing total protein, suggesting mild oxidative stress. Montelukast-containing combinations primarily modulate hydrogen peroxide without major effects on protein content or overall antioxidant capacity. These findings indicate that drug combinations exert differential effects on lung oxidative homeostasis, highlighting the need for careful evaluation of pulmonary redox status during combination therapy.