DIETARY SILICON AFFECTS ACID AND ALKALINE-PHOSPHATASE AND CALCIUM-45 UPTAKE IN BONE OF RATS

Silicon (Si) apparently is involved in bone calcification; however, it s exact role is unclear. Thus, the effect of Si on bone turnover and b one formation was investigated by utilizing a 2 x 2 factorially arrang ed experiment. Groups of 12 animals were fed Si-deficient (0.6 mu g/g) or Si-adequate (35 mu g/g) casein/ground corn diets for 9 wk. At 7 wk , six animals from each group were implanted subcutaneously in the tho racic region with a gelatin capsule containing 30 mg of demineralized bone (DB) and another capsule containing 70 mg mineralized bone (MB) o btained from rats fed Si-low (1.2 mu g/g) diets; the remaining animals were implanted similarly but the source of DB and MB was rats fed Si- supplemented (50 mu g/g) diets. The animals were intraperitoneally inj ected with 0.1 mu Ci Ca-45/g body weight 14 h before the end of the ex periment which was 14 d after the capsules were implanted. Marker enzy me activities (alkaline-formation and acid-resorption phosphatases) an d the uptake of Ca-45 by femur and bone implants were measured. Both b one turnover and bone formation as indicated by acid phosphatase and a lkaline phosphatase were higher in femurs of Si-adequate than Si-defic ient rats. Neither dietary Si nor source of bone for the MB or DB impl ants affected ectopic bone formation; however, an interaction between Si and implant bone source affected acid phosphatase in both MB and DB implants. Silicon did not affect Ca-45 uptake by femur, but uptake by both MB and DB implants was increased by dietary Si supplementation. The bone implants significantly decreased calcium and increased copper concentrations in the tibia when the source of bone was animals fed S i-adequate diets. The decreased activity of alkaline and acid phosphat ase in femur bone, the decreased uptake of Ca-45 in ectopic bone, and decreased copper concentration in tibia of Si-deprived rats is new evi dence confirming that Si affects bone metabolism. (C) 1994 Wiley-Liss, Inc.