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Montelukast ameliorates kidney function and urinary bladder sensitivity in experimentally induced renal dysfunction in rats
Author(s) -
Suddek Ghada M.
Publication year - 2013
Publication title -
fundamental and clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.655
H-Index - 73
eISSN - 1472-8206
pISSN - 0767-3981
DOI - 10.1111/j.1472-8206.2011.00996.x
Subject(s) - montelukast , nephrotoxicity , endocrinology , malondialdehyde , blood urea nitrogen , renal function , medicine , kidney , creatinine , oxidative stress , glutathione , urinary system , cisplatin , lipid peroxidation , chemistry , pharmacology , biochemistry , chemotherapy , enzyme , asthma
Effect of montelukast on the renal dysfunction induced by cisplatin was investigated. A single dose of cisplatin (7 mg/kg, i.p.) induced nephrotoxicity, which was manifested by increasing the sensitivity of isolated urinary bladder rings to acetylcholine (ACh) together with a significant elevation of serum creatinine, blood urea nitrogen, and lactate dehydrogenase. On the other hand, serum albumin was significantly decreased. Moreover, renal dysfunction was further confirmed by a significant increase in lipid peroxides that were measured as malondialdehyde (MDA) in kidney tissue homogenate. Kidney reduced glutathione (GSH) content and superoxide dismutase (SOD) activity were measured, which were decreased and increased, respectively. Administration of montelukast (10 mg/kg/day, p.o.) 5 days before and 5 days after cisplatin injection significantly ameliorated the renotoxic effects of cisplatin, as judged by a significant reduction in the responses of isolated bladder rings to ACh. The deleterious changes induced by cisplatin treatment in kidney function parameters and oxidative stress markers were significantly mitigated by montelukast treatment. Conclusion: Montelukast may be a beneficial remedy for cisplatin‐induced renal dysfunction.