title: Oxidant damage in Kashin-Beck disease and a rat Kashin-Beck disease model by employing T-2 toxin treatment under selenium deficient conditions.
abstract: 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.
authors.affiliation: Institute of Endemic Diseases, Xi'an Jiaotong University College of Medicine, Shaanxi, PR China.
authors.forename: Jing-hong
authors.initials: JH
authors.lastname: Chen
authors.forename: Senghai
authors.initials: S
authors.lastname: Xue
authors.forename: Siyuan
authors.initials: S
authors.lastname: Li
authors.forename: Zhi-lun
authors.initials: ZL
authors.lastname: Wang
authors.forename: Haojie
authors.initials: H
authors.lastname: Yang
authors.forename: Wei
authors.initials: W
authors.lastname: Wang
authors.forename: Daiqing
authors.initials: D
authors.lastname: Song
authors.forename: Xiaorong
authors.initials: X
authors.lastname: Zhou
authors.forename: Chen
authors.initials: C
authors.lastname: Chen
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D002356:Cartilage / Q000378:metabolism; D002358:Cartilage, Articular / Q000473:pathology; D002374:Catalase / Q000378:metabolism; D002648:Child; D002675:Child, Preschool; D004195:Disease Models, Animal; D005979:Glutathione Peroxidase / Q000378:metabolism; D006801:Humans; D057767:Kashin-Beck Disease / Q000503:physiopathology*; D015227:Lipid Peroxidation; D008297:Male; D018384:Oxidative Stress; D051381:Rats; D017207:Rats, Sprague-Dawley; D012643:Selenium / Q000172:deficiency*; D013482:Superoxide Dismutase / Q000378:metabolism; D013605:T-2 Toxin / Q000633:toxicity*; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
chemical_list: D000975:Antioxidants; D017392:Thiobarbituric Acid Reactive Substances; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D012643:Selenium; D013605:T-2 Toxin