Beneficial Effects of Montelukast Against Methotrexate-Induced Liver Toxicity: A Biochemical and Histological Study

The effects of montelukast against methotrexate-induced liver damage were investigated. 35 Wistar albino female rats were divided into 5 groups as follows: group I: control; group II: montelukast (ML); group III: methotrexate (Mtx); group IV: montelukast treatment after methotrexate application (Mtx + ML); group V: montelukast treatment before methotrexate application (ML + Mtx). At the end of the experiment, the liver tissues of rats were removed. Malondialdehyde (MDA), myeloperoxidase (MPO), and reduced glutathione levels were determined from liver tissues. In addition, the liver tissues were examined histologically. MDA and MPO levels of Mtx group were significantly increased when compared to control group. In Mtx + ML group, these parameters were decreased as compared to Mtx group. Mtx injection exhibited major histological alterations such as eosinophilic staining and swelling of hepatocytes. The glycogen storage in hepatocytes was observed as decreased by periodic acid schiff staining in Mtx group as compared to controls. ML treatment did not completely ameliorate the lesions and milder degenerative alterations as loss of the glycogen content was still present. It was showed that montelukast treatment after methotrexate application could reduce methotrexate-induced experimental liver damage

Therapeutic and protective effects of montelukast against doxorubicin-induced acute kidney damage in rats

Objective(s): The current study was designed to investigate the therapeutic and protective effects of montelukast (ML) against doxorubicin (DOX)-induced acute kidney damage in rats.Materials and Methods: Thirty-five Wistar albino female rats were randomly divided into 5 groups as follows: Group I: Control; Group II: Control+ML; Group III: DOX; Group IV: DOX+ML; Group V: ML+DOX. At the end of the experiment, the kidney tissues of rats were collected. Thiobarbituric acid reactive substance (TBARS), reduced glutathione, superoxide dismutase (SOD), and catalase levels were determined from the kidney tissues. In addition, the kidney tissues were examined histologically.Results: DOX induced a significant increase in the kidney TBARS levels, whereas SOD contents significantly decreased when compared with the control group.  On the other hand, ML administration before and after DOX injection caused significant decreases in TBARS production and also increases in SOD levels. Histologically, the most remarkable damage was glomerulosclerosis and tubular changes in the DOX group. Moreover, marked tubular necrosis and swelling in tubular epithelial cells were observed in this group. Contrarily, although glomerulosclerosis was recognized as alleviated also in both DOX+ML and ML+DOX groups, the lesions did not completely ameliorate. However, treatment with ML after DOX injection was more effective than treatment with ML before DOX injection with respect to the protection of tubular structures. Conclusion: It was determined that ML treatment after DOX injection caused therapeutic effects against DOX-induced kidney damage. Thence, ML treatment is of some clinical properties for oxidative stress damage in kidney tissues