Objective: Montelukast, an asthma drug, has an anti-inflammatory effect on tissues. We aimed to investigate therapeutic effect of montelukast (MK) on acetaminophen (APAP) - induced renal damage in rat models.
Material and Methods: Twenty-four rats were randomly divided into four groups of six animals each. APAP was administered intraperitoneally as a single dose of 1000 mg/kg/day. In the treatment group, MK dose was 10 mg/kg and administered by oral gavage after APAP. The other groups were APAP + Saline group and the control group. We measured tissue malondialdehyde (MDA), reduced glutathione (GSH), and Nitric oxide (NO) levels to determine the nephrotoxicity.
Results: Serum Blood Urea Nitrogen (BUN) and creatinine levels were measured significantly higher in APAP group than rats in the control and APAP + MK groups. The level of GSH was significantly diminished in APAP-treated rats. However, the administration of MK significantly increased the level of GSH in the MK treatment group. Tissue MDA levels in rats treated with APAP alone were significantly higher compared to the control group and APAP + MK group. The level of NO was measured as elevated in APAP treated group. However, NO levels in the MK treatment group were significantly lower than APAP treated group. Furthermore, some morphological recoveries were observed in the MK treatment group compared to APAP alone group.
Conclusion: MK has beneficial effects on APAP-induced renal toxicity and dysfunction. However, clinical studies are needed to demonstrate appropriate use and effects.
Keywords: Acetaminophen, Kidney, Montelukast, Nephrotoxicity, Oxidative stress
ABSTRACT
Objective: Montelukast, an asthma drug, has an anti-inflammatory effect on tissues. We aimed to investigate therapeutic effect of montelukast (MK) on acetaminophen (APAP) - induced renal damage in rat models.
Material and Methods: Twenty-four rats were randomly divided into four groups of six animals each. APAP was administered intraperitoneally as a single dose of 1000 mg/kg/day. In the treatment group, MK dose was 10 mg/kg and administered by oral gavage after APAP. The other groups were APAP + Saline group and the control group. We measured tissue malondialdehyde (MDA), reduced glutathione (GSH), and Nitric oxide (NO) levels to determine the nephrotoxicity.
Results: Serum Blood Urea Nitrogen (BUN) and creatinine levels were measured significantly higher in APAP group than rats in the control and APAP + MK groups. The level of GSH was significantly diminished in APAP-treated rats. However, the administration of MK significantly increased the level of GSH in the MK treatment group. Tissue MDA levels in rats treated with APAP alone were significantly higher compared to the control group and APAP + MK group. The level of NO was measured as elevated in APAP treated group. However, NO levels in the MK treatment group were significantly lower than APAP treated group. Furthermore, some morphological recoveries were observed in the MK treatment group compared to APAP alone group.
Conclusion: MK has beneficial effects on APAP-induced renal toxicity and dysfunction. However, clinical studies are needed to demonstrate appropriate use and effects.
Keywords: Acetaminophen, Kidney, Montelukast, Nephrotoxicity, Oxidative stress