大骨节病病因及病理过程的医化学探讨

Medicochemical studies relevent to the etiological and pathological processes of Kashin-Beck's Disease

根据大骨节病病因学及病理学过程的医化学和其他有关研究提出一个解释该病发展的新概念。活性氧自由基被认为是触发剂。它们损伤软骨细胞及细胞外基质并引起软骨细胞反分化。这些异常细胞由合成Ⅱ型胶原蛋白转为合成Ⅰ型。水中有毒有机物和真菌污染粮食中的毒素为自由基源。在其作用下形成有Ⅰ型胶原存在、蛋白多糖少、分子量低、有序性低的异常基质。后者影响羟基磷灰石矿化。这一异常细胞-异常基质-异常矿化模型可用以解释本病各种病理表现。硒及锌化合物可抑制这一病理过程。

To the authors,their experiments provoked a new concept on the developmentand progression of the disease.Free oxy-radicals are considered to be thetrigger mechanism in causing damage to the chondrocytes and extra-cellular ma-trix,and impedance to the differentiation of chondrocytes。The abnormal cellssynthesize Type Ⅰ instead of Type Ⅱ collagen。Texic erganic compounds in poabletwater and fungus-toxin(s)in polluted cereals are cons indered to be sourcesof the free oxy-radicals.Under their infleuence,the abnormal matrix,char-acterized by synthesis of Type Ⅰ cellage low in proteoglycan,histological organ-ization and molecular weight,is produced.The abnormal matrix also affectsminer alization of hydroxyapatite,the main bio-mineral bone.This cell-abno-rmal,matrix-abnormal and mineralization-abnormal model simulates very muchthe pathological features seen in clinical Kashin-Beck's disease.Selenium and zinccompounds are effective in inhibition of the pathological process.