Abstract
N-acetylcysteine (NAC), a cell membrane permeable antioxidant, is a precursor of glutathione that can remove the excess free radical and protect cells from damage by oxidative stress. Our previously study has indicated that the CHO-K1 cells undergo apoptosis after UV irradiation. The CHO-K1 cells do not express p21wafl, and the UV-induced apoptosis can be inhibited by ectopic expression of human p21wafl gene in the cells. In this study, we found that NAC could protect the cells from the UV-induced apoptosis. Although NAC might increase the intracellular glutathione (GSH) content, the inhibitory effect of NAC on the UV-induced apoptosis was probably not mediated by GSH. Adding GSH into cells failed to produce the similar effect seen with NAC. Moreover, using DL-buthionine-[S,R]-sulfoximine (BSO) to deplete the intracellular GSH content was unable to enhance the UV-induced apoptosis. Despite the large increase of the intracellular ROS content following BSO treatment, the finding that BSO could not promoter the UV-induced apoptosis suggests that the UV-induced apoptosis did not correlate with the intracellular ROS content. In addition, roscovitine, a selective cyclin-dependent kinase (CDK) inhibitor, also inhibited the UV-induced apoptosis in CHO-K1 cells. As NAC was a strong cell cycle inhibitor at G1. The inhibition of NAC upon the UV-induced apoptosis is probably mediated by the modulation of CDK activity as seen with roscovitine.