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The anabolic effect of 17β-estradiol in osteoblastic MC3T3-E1 cells was investigated. The cells were cultured for 3 days in the medium containing either vehicle or 17β-estradiol (10 -10 M). 17β-Estradiol significantly increased alkaline phosphatase activity and protein concentration in the cells. The steroid (10 M) also significantly elevated the cell numbers and the cellular DNA content. The anabolic effect by 17β-estradiol was blocked by the presence of dipicolinate (10 M), a chelator of zinc ion, suggesting a role of cellular zinc in osteoblastic cell function. The presence of zinc sulfate (10 M) or β-alanyl-L-histidinato zinc (AHZ) (10 M) significantly enhanced the 17β-estradiol (10 or 10 M)-induced increase of alkaline phosphatase activity and protein concentration in the cells; the effect of AHZ was greater than that of zinc sulfate. The enhancement by zinc compounds was not based on the augmentation of osteoblastic cell numbers. The co-addition of cycloheximide (10 M), an inhibitor of protein synthesis, completely blocked the zinc compound (10 M)-induced enhancement of 17β-estradiol's (10 M) effect to increase alkaline phosphatase activity and protein concentration in the cells. Moreover, the anabolic effect of 17β-estradiol together with or without zinc compounds was abolished by the presence of staurosporine (10 M), an inhibitor of protein kinase C, or of okadaic acid (10 M), an inhibitor of protein phosphatase. The present study demonstrates that the anabolic effect of 17β-estradiol is enhanced by zinc-chelating dipeptide in osteoblastic MC3T3-E1 cells, and that the enhancing effect may involve protein synthesis and protein kinase activity.

The inhibitory effect of zinc compounds on osteoclast-like cell formation in mouse marrow culture in vitro was characterized. The bone marrow cells were cultured for 7 days in alpha-minimal essential medium containing a well-known bone resorbing agent, 1,25-dihydroxyvitamin D3[1,25(OH)2D3] or prostaglandin E2 (PGE2). Osteoclast-like cell formation was estimated by staining for tartrate-resistant acid phosphatase (TRACP), a marker enzyme of osteoclasts. The presence of 1,25(OH)2D3 (10(-8) M) or PGE2 (10(-6) M) induced a remarkable increase in osteoclast-like multinucleated cells. These increases were enhanced by the presence of dexamethasone (10(-9) to 10(-6) M). The dexamethasone (10(-7) M)-enhanced osteoclast-like cell formation was not inhibited by the presence of zinc sulfate (10(-6) M) or zinc-chelating dipeptide (beta-alanyl-L-histidinato zinc; 10(-6) M), although the zinc compounds had an inhibitory effect on osteoclastic formation in the absence of the steroid. The effect of dexamethasone was not seen, when the steroid was added at the later stage of culture with bone-resorbing agents. In this case, the inhibitory effect of zinc compounds was clearly revealed. This effect of zinc compounds disappeared in the presence of Ca2+-chelating agent (0.5 mM EGTA). The present study suggests that zinc compounds have an inhibitory effect at the stage of differentiation of preosteoclastic cells in bone marrow cell culture system.