The biological agent rituximab ameliorates DNA damage and repair efficiency in the somatic cells of arthritic mice
Background: Rheumatoid arthritis (RA) is an autoimmune disorder that deteriorates joints and can affect various physiological systems if not properly managed. The persistent joint inflammation and oxidative damage caused by RA can lead to genomic instability, a primary feature of most cancer cells....
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| Format: | Article |
| Language: | English |
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Elsevier
2025-07-01
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| Series: | Electronic Journal of Biotechnology |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S0717345825000168 |
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| author | Mohammed A. Al-Hamamah Mohamed A. Mahmoud Moureq R. Alotaibi Ahmed Nadeem Mushtaq A. Ansari Sheikh F. Ahmad Saleh A. Bakheet Gamaleldin I. Harisa Sabry M. Attia |
| author_facet | Mohammed A. Al-Hamamah Mohamed A. Mahmoud Moureq R. Alotaibi Ahmed Nadeem Mushtaq A. Ansari Sheikh F. Ahmad Saleh A. Bakheet Gamaleldin I. Harisa Sabry M. Attia |
| author_sort | Mohammed A. Al-Hamamah |
| collection | DOAJ |
| description | Background: Rheumatoid arthritis (RA) is an autoimmune disorder that deteriorates joints and can affect various physiological systems if not properly managed. The persistent joint inflammation and oxidative damage caused by RA can lead to genomic instability, a primary feature of most cancer cells. In RA, the prevalence of malignancy is comparatively higher than in the general population. However, it is unclear if the disease itself or its treatments induce susceptibility to neoplastic disorders. Our goal was to study genomic instability in the arthritic mouse model, namely DNA damage and repair and determine if the long-term use of the biological agent rituximab can impact these changes. Results: Our results show that rituximab did not disrupt genomic stability at the tested regimen. Arthritic mice had more spontaneous DNA damage and a slower repair rate than control mice. Redox imbalance, oxidative DNA damage, and disturbance in the DNA repair pathways are also increased in arthritic mice. Meanwhile, rituximab treatment reduced oxidative DNA damage and accelerated DNA repair rate, improving redox balance and restoring the disturbances in the DNA repair gene expression at both mRNA as determined by RT2 Profiler PCR array and protein levels as determined by Western blotting analysis in arthritic animals. Additionally, the ameliorative effect of rituximab has also been shown by its ability to reduce the severity of joint inflammation and histopathological alterations induced by arthritis. Conclusions: The findings indicate that rituximab is a non-genotoxic, safe, effective drug for the treatment of RA and its complications.How to cite: Al-Hamamah MA, Mahmoud MA, Alotaibi MR, et al. The biological agent rituximab ameliorates DNA damage and repair efficiency in the somatic cells of arthritic mice. Electron J Biotechnol 2025;76. https://doi.org/10.1016/j.ejbt.2025.03.004. |
| format | Article |
| id | doaj-art-01cb35ec95c94e3fb9a6f76a724a496e |
| institution | Matheson Library |
| issn | 0717-3458 |
| language | English |
| publishDate | 2025-07-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Electronic Journal of Biotechnology |
| spelling | doaj-art-01cb35ec95c94e3fb9a6f76a724a496e2025-07-13T04:53:35ZengElsevierElectronic Journal of Biotechnology0717-34582025-07-01766778The biological agent rituximab ameliorates DNA damage and repair efficiency in the somatic cells of arthritic miceMohammed A. Al-Hamamah0Mohamed A. Mahmoud1Moureq R. Alotaibi2Ahmed Nadeem3Mushtaq A. Ansari4Sheikh F. Ahmad5Saleh A. Bakheet6Gamaleldin I. Harisa7Sabry M. Attia8Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, 11451 Riyadh, Saudi ArabiaDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, 11451 Riyadh, Saudi ArabiaDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, 11451 Riyadh, Saudi ArabiaDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, 11451 Riyadh, Saudi ArabiaDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, 11451 Riyadh, Saudi ArabiaDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, 11451 Riyadh, Saudi ArabiaDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, 11451 Riyadh, Saudi ArabiaDepartment of Pharmaceutics, College of Pharmacy, King Saud University, 11451 Riyadh, Saudi ArabiaDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, 11451 Riyadh, Saudi Arabia; Corresponding author.Background: Rheumatoid arthritis (RA) is an autoimmune disorder that deteriorates joints and can affect various physiological systems if not properly managed. The persistent joint inflammation and oxidative damage caused by RA can lead to genomic instability, a primary feature of most cancer cells. In RA, the prevalence of malignancy is comparatively higher than in the general population. However, it is unclear if the disease itself or its treatments induce susceptibility to neoplastic disorders. Our goal was to study genomic instability in the arthritic mouse model, namely DNA damage and repair and determine if the long-term use of the biological agent rituximab can impact these changes. Results: Our results show that rituximab did not disrupt genomic stability at the tested regimen. Arthritic mice had more spontaneous DNA damage and a slower repair rate than control mice. Redox imbalance, oxidative DNA damage, and disturbance in the DNA repair pathways are also increased in arthritic mice. Meanwhile, rituximab treatment reduced oxidative DNA damage and accelerated DNA repair rate, improving redox balance and restoring the disturbances in the DNA repair gene expression at both mRNA as determined by RT2 Profiler PCR array and protein levels as determined by Western blotting analysis in arthritic animals. Additionally, the ameliorative effect of rituximab has also been shown by its ability to reduce the severity of joint inflammation and histopathological alterations induced by arthritis. Conclusions: The findings indicate that rituximab is a non-genotoxic, safe, effective drug for the treatment of RA and its complications.How to cite: Al-Hamamah MA, Mahmoud MA, Alotaibi MR, et al. The biological agent rituximab ameliorates DNA damage and repair efficiency in the somatic cells of arthritic mice. Electron J Biotechnol 2025;76. https://doi.org/10.1016/j.ejbt.2025.03.004.http://www.sciencedirect.com/science/article/pii/S0717345825000168Anti-CD20 monoclonal antibodyArthritic miceAutoimmune diseaseDNA damageDNA repairGenomic instability |
| spellingShingle | Mohammed A. Al-Hamamah Mohamed A. Mahmoud Moureq R. Alotaibi Ahmed Nadeem Mushtaq A. Ansari Sheikh F. Ahmad Saleh A. Bakheet Gamaleldin I. Harisa Sabry M. Attia The biological agent rituximab ameliorates DNA damage and repair efficiency in the somatic cells of arthritic mice Electronic Journal of Biotechnology Anti-CD20 monoclonal antibody Arthritic mice Autoimmune disease DNA damage DNA repair Genomic instability |
| title | The biological agent rituximab ameliorates DNA damage and repair efficiency in the somatic cells of arthritic mice |
| title_full | The biological agent rituximab ameliorates DNA damage and repair efficiency in the somatic cells of arthritic mice |
| title_fullStr | The biological agent rituximab ameliorates DNA damage and repair efficiency in the somatic cells of arthritic mice |
| title_full_unstemmed | The biological agent rituximab ameliorates DNA damage and repair efficiency in the somatic cells of arthritic mice |
| title_short | The biological agent rituximab ameliorates DNA damage and repair efficiency in the somatic cells of arthritic mice |
| title_sort | biological agent rituximab ameliorates dna damage and repair efficiency in the somatic cells of arthritic mice |
| topic | Anti-CD20 monoclonal antibody Arthritic mice Autoimmune disease DNA damage DNA repair Genomic instability |
| url | http://www.sciencedirect.com/science/article/pii/S0717345825000168 |
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