Methotrexate reduces the levels of pentosidine and 8-hydroxy-deoxy guanosine in patients with rheumatoid arthritis
| Autor: | Akira Nagano, Tetsuyuki Nagafusa, Yasunori Kageyama, Eiji Torikai, Masaaki Takahashi |
|---|---|
| Rok vydání: | 2007 |
| Předmět: |
musculoskeletal diseases
medicine.medical_specialty Time Factors Urinary system Arthritis medicine.disease_cause Arginine Arthritis Rheumatoid chemistry.chemical_compound Rheumatology Glycation Internal medicine medicine Humans Pentosidine skin and connective tissue diseases business.industry Lysine Deoxyguanosine medicine.disease Oxygen Oxidative Stress Endocrinology Methotrexate Treatment Outcome chemistry 8-Hydroxy-2'-Deoxyguanosine Rheumatoid arthritis Antirheumatic Agents Creatinine Immunology Joints business Reactive Oxygen Species Oxidative stress medicine.drug DNA Damage |
| Zdroj: | Modern rheumatology. 17(5) |
| ISSN: | 1439-7595 |
| Popis: | This study was performed to investigate whether methotrexate (MTX) affects the levels of oxidative stress markers, including pentosidine one of the glycation end products (AGEs) or 8-hydroxy-deoxy guanosine (8-OHdG). These stress markers represent DNA damage; 19 rheumatoid arthritis (RA) patients underwent MTX treatment. The levels of serum total, urinary total, urinary-free pentosidine and also urinary 8-OHdG, as well as clinical parameters, including disease activity scores for 28 joints (DAS28) were measured at baseline and at 3 and 6 months after the initial treatment with MTX. After the initial treatment with MTX, serum total and urinary total pentosidine levels were reduced at 6 months, and urinary-free pentosidine levels were reduced at 3 and 6 months. Urinary 8-OHdG levels also were significantly reduced at 6 months after the initial treatment with MTX. This study demonstrated that MTX plays a role as a regulator against pentosidine formation and oxidative DNA damage in RA patients. |
| Databáze: | OpenAIRE |
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