摘要
研究了在·OH与病区饮水中黄腐酸(FA)造成损伤的猪软骨Ⅱ型胶原蛋白中羟基磷灰石(HAP)成长的动力学,并与未损伤的胶原蛋白比较。结果表明,正常情况下的Ⅱ型胶原蛋白抑制HAP成长,而氧化性降解损伤的Ⅱ型胶原蛋白促进HAP成长,但反应均为二级。X射线分析及扫描电镜观察发现,损伤的Ⅱ型胶原蛋白使HAP成长初期结晶性差,最终所得结晶聚合度大。提示软骨组织中的Ⅱ型胶原蛋白因氧化降解后表现了促矿化的性质,这与大骨节病的发生发展可能有重要联系。
To clarify the effects of free radical damaged Type Ⅱ collagen on the mineralization process in cartilage, the kinetics of crystal growth of hydroxyapatite in presence of collagenll from pig cartilage, intact and damaged by. OH and fulvic acid from potable water in epidemic region. The experimental results show that the normal Type Ⅱ collagen inhibits the crystal growth, which is characterized by a lower ks value relative to that obtained in the absence of collagen. In case of the damaged collagens, the crystal growth is accelerated. Nevertheless, all the reactions are of second order. The X-ray diffraction analysis and SEM show that in all cases, the solid phases are attributed to hydroxyapatite, but the damaged Type Ⅱ collage causes the apatite of lower crystallinity and higher agglomeration. These results indicate that the abnormal biomineralization in abnormal cartilage matrix might be an important clue in pathological process in Kaschin-Beck disease.
出处
《北京医科大学学报》
CSCD
1989年第5期393-396,共4页
Journal of Peking University(Health Sciences)
基金
"七五"攻关项目75-62-03-07-01专题
关键词
胶原蛋白
羟基磷灰石
大骨节病
free radical Fulric acid Collagen Mineralization Hydroxyapatite
