Authors
Abdul Rehman, Muhammad Jamil, Maham Farhan, Amna Saleem Khan, Mahroo Javaid, Aqsa Iftikhar, Uzma Urooj Malik
Published in
Pakistan journal of medical sciences. Volume 42. Issue 8. Pages 2066-2071.
Abstract
Osteoarthritis (OA) and Rheumatoid Arthritis (RA) are chronic, degenerative and inflammatory joint diseases, aggravated by reactive oxygen species (ROS) and impaired antioxidant defense system. However, gender based oxidative stress analysis remain under-examined, despite increasing evidence points towards sex-based biochemical changes in arthritis patients. The study aimed to measure the antioxidant activities of enzymes including superoxide dismutase (SOD), Glutathione reductase (GR) alongside reduced glutathione (GSH), and catalase (CAT) in female arthritis patients. Calcium balance is also estimated in order to analyze the bone demineralization.
The case-control study was designed and conducted at the Orthopedic Department of a Dr. Ruth K. M. Pfau, Civil hospital, Karachi. Serum levels of GSH, GR, SOD, CAT, and calcium were evaluated in 42 arthritis patients and 16 age matched healthy female controls by using standard spectrophotometric and biochemical assays. Data was expressed as mean ± SD and analyzed statistically to compare both the groups.
Arthritis patients in comparison with healthy controls showed significant decrease in GSH (p < 0.001) and GR (p < 0.01) levels, while SOD and CAT levels were slightly reduced but non-significant. Similarly, slightly higher calcium levels were also observed, suggesting altered mineral homeostasis associated with inflammatory conditions. The simultaneous decrease in antioxidant enzyme activities suggests the impaired redox homeostasis in female patients.
The study highlights an altered antioxidant status and disturbed calcium homeostasis in female patients. These alterations in biochemical system suggest the therapeutic potential of antioxidant and calcium modulating interventions as effective treatment for managing and slowing disease progression in females.
PMID:
42668919
Bibliographic data and abstract were imported from PubMed on 30 Aug 2026.
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