Details

Autor(en) / Beteiligte

• Chen, Jing-hong
• Xue, Senghai
• Li, Siyuan
• Wang, Zhi-lun
• Yang, Haojie
• Wang, Wei
• Song, Daiqing
• Zhou, Xiaorong
• Chen, Chen

Titel

Oxidant damage in Kashin-Beck disease and a rat Kashin-Beck disease model by employing T-2 toxin treatment under selenium deficient conditions

Ist Teil von

• Journal of orthopaedic research, 2012-08, Vol.30 (8), p.1229-1237

Ort / Verlag

Hoboken: Wiley Subscription Services, Inc., A Wiley Company

Erscheinungsjahr

2012

Link zum Volltext

Quelle

Wiley Online Library Journals Frontfile Complete

Beschreibungen/Notizen

• Kashin‐Beck disease (KBD) is an endemic degenerative osteoarthropathy, but the mechanisms underlying its pathogenesis remains unclear. This study compares antioxidant capacity and lipid peroxidation using a novel model, in which rats were administered a selenium‐deficient diet for 4 weeks prior to their exposure to T‐2 toxin for 4 weeks. Changes in cell morphology and empty chondrocyte lacunae indicative of cell death, as well as cartilage proteoglycan loss in the deep zone of articular cartilage of knee joints were observed in rats with selenium‐deficient diet plus T‐2 toxin treatment. These changes were similar to those observed previously in KBD. The levels of thiobarbituric acid reactive substances (TBARS), indicative of lipid peroxidation in serum and cartilage, were significantly increased in all experimental groups compared to the normal diet group, while the levels of antioxidants, measured as total antioxidant capacity (T‐AOC), catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidases (GPX), in serum and cartilage were significantly lower than that in the normal diet group. The mRNA expression of those antioxidants in cartilage tissue was significantly reduced by T‐2 toxin alone or by selenium‐deficient diet plus T‐2 toxin treatment. These results indicate that increasing TBARS and decreasing antioxidants in serum and cartilage by T‐2 toxin treatment with a selenium‐deficient nutritional status may alter oxidative stress in joint tissues and contribute to the pathological process of cartilage damage in KBD. © 2012 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 30:1229–1237, 2012