Russell J E, Avioli L V
J Clin Invest. 1972 Dec;51(12):3072-9. doi: 10.1172/JCI107134.
The effect of chronic renal disease on bone matrix and mineral maturation was evaluated in rats with experimental renal insufficiency of 2-11 wk duration utilizing bromoform-toluene gradient fractionation of bone powder, pulse labeling experiments with (45)Ca and proline-(3)H differential extraction, and X-ray diffraction techniques.Maturation defects in both collagen and mineral ((45)Ca) metabolism were documented as early as 2 wk after the induction of uremia, when total bone calcium, inorganic phosphate, and hydroxyproline content were unchanged. The maturational defect progressed with advancing uremia despite insignificant changes in plasma pH and calcium, and normal bone carbonate levels. Although circulating levels of 25-hydroxycholecalciferol were significantly lower than normal in the uremic animals, pretreatment with either this vitamin D metabolite or vitamin D(3) itself failed to alter the observed changes in skeletal maturation.
利用骨粉的溴仿 - 甲苯梯度分级、用(45)钙和脯氨酸 -(3)氢差异提取进行脉冲标记实验以及X射线衍射技术,在持续2 - 11周实验性肾功能不全的大鼠中评估了慢性肾病对骨基质和矿物质成熟的影响。早在尿毒症诱导后2周就记录到了胶原蛋白和矿物质((45)钙)代谢的成熟缺陷,此时总骨钙、无机磷酸盐和羟脯氨酸含量未发生变化。尽管血浆pH值、钙和正常骨碳酸盐水平变化不显著,但随着尿毒症的进展,成熟缺陷仍在加剧。虽然尿毒症动物体内25 - 羟基胆钙化醇的循环水平显著低于正常水平,但用这种维生素D代谢产物或维生素D3本身进行预处理未能改变观察到的骨骼成熟变化。