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Effects of Nutritional Copper Deficiency on the Biomechanical Properties of Bone and Arterial Elastin Metabolism in the Chick^{1, 2,}

Department of Nutrition, College of Agricultural and Environmental Sciences, and Department of Orthopaedic Surgery, School of Medicine, University of California, Davis, California 95616

Increased bone fragility was observed in chickens fed diets containing < 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.

KEY WORDS: • bone • elastin • copper • connective tissue

¹ Supported in part by grants from the Riverside and Sacramento-Yolo-Sierra Heart Association and USPHS research grants HL-15965 and AM-14403.

² Address reprint requests to either R. B. Rucker or R. S. Riggins.

Manuscript received 12 February 1975.

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