N-acetyl-L-cysteine (NAC)是一個著名的抗氧化劑，NAC的氧化還原能力，可以清除細胞中過多的氧化自由基，使細胞免於氧化自由基造成的傷害。本篇論文中增生中的中國倉鼠卵巢細胞K1(CHO-K1)處理NAC後，發現NAC會抑制細胞的增生和改變細胞的形態，隨著處理時間的增加，細胞的形態由正常的紡錘形漸漸變為圓形，但是靜止期的CHO-K1細胞處理NAC，則看不到細胞形態改變的現象。當NAC由培養液中移除，隨著時間的增加，則受到改變的細胞形態又逐漸恢復成為正常的紡錘形，且受到延遲的細胞週期也重新再進行，證實NAC產生的效應是具有可恢復性的。增生細胞核抗原(Proliferating cell nuclear antigen, PCNA)是DNA聚合脢δ和ε的輔助因子，在真核細胞的DNA合成及DNA的切除修補上是必需的。增生細胞核抗原的基因表現受生長調節，也會因某些胞外的刺激而產生變化。我們發現，紫外線-C照射CHO-K1細胞，不論細胞是處於有、無血清的環境下，均會誘發細胞PCNA 基因的表現。為了減少血清對PCNA表現的促進效應，本文中使用無血清的培養液，在紫外線-C的照射前、後給予NAC的處理，發現受紫外線-C所誘發的PCNA訊息RNA和蛋白質表現會受到NAC的抑制。此外NAC是GSH的前驅物，所以我們外加GSH模擬NAC的效應，發現NAC的抑制效應和NAC提高細胞內的GSH量無關。由以上的結果顯示，NAC抑制CHO-K1細胞的增生和參與紫外線-C所造成的PCNA表現的調控。

N-acetyl-L-cysteine (NAC), a well-known antioxidant is a scavenger of free radicals that can remove excess free radicals from cells and protect cells from damage by oxidants. In cycling CHO-K1 cells, NAC can inhibit the proliferation of cells, delay the procession of cell cycle and change the morphology of cells. When the cells are treated by NAC, the morphology of cells changes from normal spindle to abnormal round gradually. But we can't find the morphology change on quiescent cells. When the medium containing NAC is removed, cell cycle will go ahead and the change of cell morphology will reverse. Proliferating cell nuclear antigen (PCNA), an auxiliary factor of DNA polymerase δ□andε, is required for eukaryotic cell DNA synthesis and excision repair. Expression of PCNA is growth regulated but can be induced by variable extracellular stimuli including exposure to UV irradiation. We have found that UV-C irradiation can induce PCNA gene expression in CHO.K1 cells, no matter recovering in serum or in serum-free medium. To exclude the effect of serum stimulation, we have treated quiescent cells with NAC before and after UV-C irradiation under serum free condition. We find that NAC can inhibit UV-C induction of PCNA mRNA and protein. Although NAC is a GSH precursor, the inhibitory effect of UV induction of PCNA seems to GSH independent. The results suggest that NAC involves in anti-proliferation of CHO.K1 cells and regulation of UV-C response of PCNA.

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