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Biomedical subjects

R B Rucker

Publications and source records attributed to R B Rucker.

At least 109 records · Page 6Linked to original sources

Effects of fluoride and ethane-1-hydroxy-1,1-diphosphonate on bone metabolism in the growing chick.

White Leghorn cockerols were fed a semipurified diet (containing fluoride at 0 to 800 ppm) from the day of hatching. The birds were also injected daily with solutions containing ethane-1-hydroxy-1,1-diphosphonate (EHDP) at concentrations ranging from 5 to 20 mg as phosphorus/kg of body weight or isotonic saline. Changes in bone mineral composition and plasma Ca, Mg and F were determined as well as alterations in bone pyrophosphatase and the amounts of bone cyclic-3',5'-adenosine monophosphate (cAMP). Since dietary fluoride in high amounts is known to stimulate new bone formation, the purpose of the study was to assess whether a potent inhibitor of mineralization, such as EHDP, might alter the response to high dietary fluoride. Although bone fluoride and magnesium were increased in relationship to dietary fluoride, the administration of EHDP had little effect on these changes at low to moderate levels of fluoride. The levels of soluble bone pyrophosphatase were not greatly influenced by changes in dietary fluoride. Administration of EHDP at 20 mg P/kg, however, typically decreased the levels of bone pyrophosphatase. Bone cAMP did not appear to be influenced by either dietary fluoride or EHDP. Using tissue culture techniques, the effects of fluoride on calcium uptake and release from embryonic chick bone were also studied. The presence of 1 mM fluoride in the medium appeared to stimulate calcium uptake and reduced calcium release from chick bone. In general, the results were in keeping with previous suggestions that the major effect of fluoride on bone is the formation of fluoroapatite and subsequent effects this may have on other metabolic alterations.

Alkaline Phosphatase↗

Effects of nutritional copper deficiency on the biomechanical properties of bone and arterial elastin metabolism in the chick.

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.

Animal Nutritional Physiological Phenomena↗