Dziak R, Vernillo A, Rifkin B
Department of Oral Biology, State University of New York, Buffalo.
J Bone Miner Res. 1988 Aug;3(4):415-20. doi: 10.1002/jbmr.5650030408.
The effects of phenytoin (diphenylhydantoin, DPH) on calcium uptake in osteoblastic cells were studied to elucidate the potential mechanism of action of this antiepileptic drug on bone metabolism. Preincubation of the human osteoblastic osteosarcomal cell line, SaOS-2, and normal rat osteoblastic cells with DPH decreased basal calcium uptake. This inhibition occurred at DPH doses from 0.1 to 50 micrograms/ml. Parathyroid hormone (PTH) and prostaglandin E2 (PGE2) increased calcium uptake in the SaOS-2 cell line. Following preincubation with DPH, calcium uptake in cells treated with PTH or PGE2 did not exceed control levels. However, significant increases in the PTH- or PGE2-treated + DPH-pretreated cells compared to DPH pretreatment alone were still observed. These studies indicate that DPH induces decreases in osteoblastic calcium influx and they add further information on the possible mode of action of this drug on bone.
研究了苯妥英（二苯乙内酰脲，DPH）对成骨细胞钙摄取的影响，以阐明这种抗癫痫药物对骨代谢的潜在作用机制。用人成骨肉瘤细胞系SaOS-2和正常大鼠成骨细胞与DPH预孵育可降低基础钙摄取。这种抑制作用在DPH剂量为0.1至50微克/毫升时出现。甲状旁腺激素（PTH）和前列腺素E2（PGE2）可增加SaOS-2细胞系中的钙摄取。用DPH预孵育后，用PTH或PGE2处理的细胞中的钙摄取未超过对照水平。然而，与单独的DPH预处理相比，在用PTH或PGE2处理+ DPH预处理的细胞中仍观察到显著增加。这些研究表明，DPH可导致成骨细胞钙内流减少，并进一步提供了关于该药物对骨可能作用方式的信息。
