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Ra ostcobasts were isolated from the 21-day fetal rat calvchas. The cells were grown in DMEM Plus 10% FBS, and were treated for 24 h. with 10 μmol/L TPEN or 10 μmol/L TPEN supplemented with 10 μmol/L Zn2+. Apoptosis of osteoblasts were measured by fiow cytometry, electron microscopy and DNA fragmentation analyzed by gel elecmphoresis. In addition, IP3 production and PKC activity were measmed in ordr to show whether they are involved in apoptosis in osteoblast induced by alnc deficiency. The results showed that 10 μmol/L TPEN could induce apoptosis in osteoblast in 24 h. But cells ed with 10μmol/L TPEN supplemented with 10 μmol/L Zn2+ showed no apoptotic changs in 24 h. TPEN significantly reduced the formation of IP3 and PKC activity after 24 h incubation. No differences were observed between the cells treated with TPEN supPlemented with Zn2+ simulaneosly and the untreated cells. It can be inferred that apoptosis induced by ainc deficiency may be due to the decreased activity of PKC which is impaired by reduced formation of IP3.
The cells were grown in DMEM Plus 10% FBS, and were treated for 24 h. With 10 μmol / L TPEN or 10 μmol / L TPEN supplemented with 10 μmol / L Zn2 + . Apoptosis of osteoblasts were measured by fiow cytometry, electron microscopy and DNA fragmentation analyzed by gel elecmphoresis. In addition, IP3 production and PKC activity were measmed in ordr to show whether they are involved in apoptosis in osteoblast induced by alnc deficiency. The results showed that 10 μmol / L TPEN could induce apoptosis in osteoblast in 24 h. But cells ed with 10 μmol / L TPEN supplemented with 10 μmol / L Zn2 + showed no apoptotic changs in 24 h. TPEN significantly reduced the formation of IP3 and PKC activity after 24 h incubation. No differences were observed between the cells treated with TPEN supPlemented with Zn2 + simulaneosly and the untreated cells. It can be inferred that apoptosis induced by ainc deficiency may be due to the decreased activity of PKC which is impaired by reduced formation of IP3.