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在温育的小牛关节软骨切片介质中加入黄嘌呤氧化酶/次黄嘌呤活性氧产生系统,可使关节软骨蛋白聚糖的降解显著增高。这种作用不能被超氧化物歧化酶或铁络合剂二乙三胺戊乙酸抑制,但可被过氧化氢酶抑制。在温育的介质中加入H_2O_2,也可使关节软骨蛋白聚糖降解增高,Cu~(2+)或Co~(2+)对此有显著促进作用,其它过渡金属则作用不明显。应用Sepharose 6B柱层析,分析软骨蛋白聚糖降解产物,多数实验组只在kD=0处有一个大分子的洗脱峰,但Cu~(2+)+H_2O_2组则在kD=0及0.57处出现两个洗脱峰(分别称为峰Ⅰ及峰Ⅱ)。醋酸纤维素薄膜双向电泳证实峰Ⅱ为硫酸软骨素,提示Cu~(2+)与H_2O_2复合物可导致蛋白聚糖分子的断裂。本研究结果可能有助于阐明某些变性型骨关节疾病的发病机理,例如因缺硒所致的大骨节病等。
The addition of a xanthine oxidase / hypoxanthine generating system to the incubated calf articular cartilage sections results in a significant increase in the degradation of the cartilage proteoglycan. This effect can not be inhibited by superoxide dismutase or the iron complexing agent diethylenetriaminepentaacetic acid, but can be inhibited by catalase. Adding H 2 O 2 into the medium could also promote the degradation of proteoglycan in cartilage, and Cu 2+ or Co 2+ could promote the activity of the proteoglycan, while other transition metals did not play a significant role. Sepharose 6B column chromatography was used to analyze the proteoglycan degradation products of cartilage. Most of the experimental groups only had a macromolecule eluting peak at kD = 0, but the k2 = 0 and 0.57 Two eluting peaks appear (peaks I and II, respectively). The two-dimensional electrophoresis of cellulose acetate film confirmed that peak II was chondroitin sulfate, suggesting that Cu 2+ and H 2 O 2 complexes could cause the cleavage of proteoglycan molecules. The results of this study may help clarify the pathogenesis of certain degenerative bone and joint diseases, such as Kashin-Beck disease caused by selenium deficiency.