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Oxidant damage in Kashin‐Beck disease and a rat Kashin‐Beck disease model by employing T‐2 toxin treatment under selenium deficient conditions
Author(s) -
Chen Jinghong,
Xue Senghai,
Li Siyuan,
Wang Zhilun,
Yang Haojie,
Wang Wei,
Song Daiqing,
Zhou Xiaorong,
Chen Chen
Publication year - 2012
Publication title -
journal of orthopaedic research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.041
H-Index - 155
eISSN - 1554-527X
pISSN - 0736-0266
DOI - 10.1002/jor.22073
Subject(s) - tbars , oxidative stress , glutathione peroxidase , lipid peroxidation , superoxide dismutase , endocrinology , medicine , cartilage , chemistry , glutathione , antioxidant , toxin , biochemistry , anatomy , enzyme
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