The molecular mechanism underlying the UVC induced apoptosis in Chinese hamster ovary cells

CB Liao, BS Tzang, YJ Chiang and YC Liu PhD

Department of Life Science, National Tsing-Hua University, Hsin-Chu, Taiwan

We have found that CHO.K1 cells, in contrast to other cells such as NIH3T3, fail to arrest at G1 and manifest apoptosis following UVC irradiation. The p53 in the cells has been shown functional in our previous study. Northern and western blot analyses indicate that p21(waf1/cip1), the general CDK inhibitor, is deficient in the CHO.K1 cells. Ectopic expression of human p21(waf1/cip1) in the cells markedly inhibits the UV induced cell death and significantly increases the survival of the irradiated cells, suggesting that the deficiency of p21(waf1/cip1) is associated with the UV induced apoptosis. While the UV induced apoptosis is exacerbated by various of cell cycle inhibitors including colcemid, mimosine and hydroxyurea, the cell death is inhibited by antioxidant agents such as azide and N-acetylcystein (NAC). While NAC may convert to glutathione (GSH) in the cells, GSH is unable to inhibit the UV induced cell death; nor the cell death is enhanced by the depletion of the endogenous GSH. Our results suggest that the deregulation of CDK but not the oxidative stress is involved in the UVC induced apoptosis in the cells.

KEY WORDS: p21(waf1/cip1), Cyclin dependent kinase, cell cycle inhibitors, N-acetylcysteine, oxidative stress.

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Paper presented at the International Symposium on Predictive Oncology and Intervention Strategies; Paris, France; February 9 - 12, 2002; in the section on Apoptosis - Molecular Mechanisms.