The purpose of this study was to invastigate the serum, liver and kidney dimethylarginine dimethylaminohydrolase-1, asymmetric dimethylarginine and inducible nitric oxide synthase levels of rats induced methotrexate toxity which causes severe complications in the organism. For this purpose, 10-12 weeks old, weighing 250-300 g, 20 Sprague Dawley male rats were used. Rats were divided two groups as control and methotrexate. No treatment was applied to the control group. Methotrexate was administered single dose 20 mg/kg/ intraperitoneal to the animals in methotrexate group. The rats were decapitated at the end of 10 days. Serum aspartate aminotransferase, alkaline phosphatase, alanine aminotransferase, urea and creatinine levels, liver, kidney and serum dimethylarginine dimethylaminohydrolase, asymmetric dimethylarginine and inducible nitric oxide synthase and malondialdehyde levels were determined. After methotrexate administration, it was determined that significantly increased serum aspartate aminotransferase (P<0.05), alkaline phosphatase, alanine aminotransferase (P<0.01), urea and creatinine levels (P<0.05) and increased serum (P<0.01), liver and kidney malondialdehyde levels (P<0.05) in methotrexate group compared to the control group. While asymmetric dimethylarginine and dimethylarginine dimethylaminohydrolase-1 levels in serum, liver and kidney tissue were not statistically significant (P>0.05), the increased in serum (P<0.05), liver and kidney inducible nitric oxide synthase levels (P<0.01) was statistically significant.

As a result, no significant difference was observed in asymmetric dimethylarginine, which has an inhibitory effect on nitric oxide synthase, and dimethylarginine dimethylaminohydrolase-1, which has a significant effect on asymmetric dimethylarginine metabolism, in liver and kidney damage caused by methotrexate.