Stimulatory effect of zinc and growth factor on bone protein component in newborn rats: enhancement with zinc and insulin-like growth factor-I.

The effect of zinc and growth factor on bone protein component in newborn rats was investigated. The characterization of protein component in the femoral-diaphyseal and metaphyseal tissue of newborn rats (3-35 days old) was examined using sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis. The diaphyseal and metaphyseal tissues of 7 days-old rats were cultured for 24 or 48 h in a medium containing either vehicle, zinc sulfate (10-4 M) or dipicolinate (10-3 M), a chelator of zinc ion, in the presence or absence of insulin-like growth factor-I (IGF-I; 10-8 M) or transforming growth factor-beta (TFG-beta; 10-10 M) with an effective concentration. Many cellular protein molecules were present in the diaphyseal and metaphyseal tissues; potent bands were seen in protein molecules with about 66 and 46 kDa. Protein molecule of about 66 kDa was greatly released in the medium cultured with the diaphyseal and metaphyseal tissues. This protein in the medium was increased by culture with zinc, IGF-I or TGF-beta. Total protein content in the medium cultured with the diaphyseal and metaphyseal tissues was significantly increased in the presence of zinc, IGF-I or TGF-beta. The IGF-I-increased medium protein content was significantly enhanced by zinc. This enhancing effect was not seen in TGF-beta. Alkaline phosphatase activity and deoxyribonucleic acid (DNA) content in the diaphyseal and metaphyseal tissues was significantly increased by culture with zinc, IGF-I or TGF-beta. The effect of IGF-I was significantly enhanced by zinc, while it was not found in TGF-beta. The effect of IGF-I or TGF-beta in increasing the bone components was seen in the presence of dipicolinate. This study demonstrates that zinc, like IGF-I and TGF-beta, can increase protein components in the femoral-diaphyseal and metaphyseal tissues of new-born rats. Zinc may especially play a role in bone growth in collaboration with IGF-I.