| Summary: | As a prescribed antioxidant, N-Acetylcysteine is used in treating disease and supportive care. However, N-acetylcysteine’s role in cancer therapy is controversial and needs to be investigated thoroughly. Presently, renal cell carcinoma is one of the most common forms of malignancy and needs new anti-cancer drugs with high efficacy and low side effect. Herein, we studied the effect of N-acetylcysteine on cell proliferation, oxidant stress, and apoptosis on human renal cell carcinoma cell line A498 and tried to understand the mechanisms driving these effects. The results show that N-acetylcysteine could enhance antioxidative activities against oxidative damage and suppress the expression of the directly apoptotic protein to inhibit apoptosis when used at low concentration (<10 mM), thereby protecting A498 cells. On the other hand, N-acetylcysteine induced oxidative stress, leading to mitochondria damage and directly activating apoptotic protein to induce apoptosis at high concentrations (>10 mM), thereby killing A498 cells. Therefore, N-acetylcysteine has two contradictory activities towards renal cell carcinoma cells.
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