Rucker R B, Riggins R S, Laughlin R, Chan M M, Chen M, Tom K
J Nutr. 1975 Aug;105(8):1062-70. doi: 10.1093/jn/105.8.1062.
Increased bone fragility was observed in chickens fed diets containing less than 1 ppm copper. Using a device that was designed to measure torsion during fracture, it could be demonstrated that bone from copper-deficient chicks fractured with less deformation and torque than bone from control chicks. The collagen of bone from copper-deficient chicks appeared to contain fewer cross-links than normal bone. The introduction of artificial cross-links into collagen from copper-deficient chick bone by formaldehyde and NaBH4 treatments improved bone strength and strain (deformation) so that it was comparable with normal bone. Copper deficiency blocks the formation of cross-links in collagens and elastin from various tissues. It is felt that the bone fragility related to nutritional copper deficiency is the result of decreased bone collagen cross linking. Arterial elastin metabolism was also investigated. By radioactively labeling arterial soluble elastin (tropoelastin) in vivo by an intraperitoneal injection of [G-3H]valine, it could be demonstrated that copper deficiency appeared to reduce its rate of metabolic turnover. Soluble elastin or tropoelastin is assumed to be the precursor of mature or insoluble elastin. The observations presented here are consistent with the view that by retarding the steps associated with elastin cross-link formation, the incorporation of soluble elastin into mature elastin may be retarded as well.
在喂食含铜量低于1 ppm日粮的鸡中观察到骨脆性增加。使用一种设计用于测量骨折时扭转力的装置，可以证明，与对照雏鸡的骨骼相比，缺铜雏鸡的骨骼在骨折时变形和扭矩较小。缺铜雏鸡骨骼的胶原蛋白似乎比正常骨骼含有更少的交联键。通过甲醛和硼氢化钠处理向缺铜雏鸡骨骼的胶原蛋白中引入人工交联键，可提高骨骼强度和应变（变形），使其与正常骨骼相当。铜缺乏会阻碍各种组织中胶原蛋白和弹性蛋白交联键的形成。人们认为，与营养性铜缺乏相关的骨脆性是骨胶原蛋白交联减少的结果。还对动脉弹性蛋白代谢进行了研究。通过腹腔注射[G-3H]缬氨酸在体内对动脉可溶性弹性蛋白（原弹性蛋白）进行放射性标记，可以证明铜缺乏似乎会降低其代谢更新率。可溶性弹性蛋白或原弹性蛋白被认为是成熟或不溶性弹性蛋白的前体。此处提出的观察结果与以下观点一致：通过延迟与弹性蛋白交联形成相关的步骤，可溶性弹性蛋白掺入成熟弹性蛋白的过程也可能受到阻碍。
