人類葡萄膜黑色素瘤是成人最常見的原位性且具致命性的眼球內惡性腫瘤，對大多數的臨床化療藥物具有高耐受性。研究顯示，三氧化二砷(arsenic trioxide)能誘發某些實體腫瘤細胞凋亡(apoptosis)。本文探討三氧化二砷對人類葡萄膜黑色素瘤細胞株M17的毒性作用，並進一步探究其分子機轉。本文用MTT法(tetrazolium test)分析，以人類皮膚纖維母細胞(fibroblast)作爲對照，發現三氧化二砷對葡萄膜黑色素瘤細胞有較明顯的知胞毒性作用，其半抑制劑量（IC50值）於M17爲1.98±0.23 μg/ml，於纖維母細胞爲122.4±4.4μg/ml。M17細胞經過l或3μg/ml三氧化二砷處理24小時後，細胞凋亡情形大量增加爲18.2及14.5倍。再者，三氧化二砷亦使caspase-3、-8及－9的活性增加，分別增加爲4.8、2.8及4.8倍，且cytochrome c表現量亦同時增加至2.1倍。綜合這些結果，我們推測三氧化二砷可經由活化caspase路徑，選譯性的引發人類葡萄膜黑色素瘤細胞產生細胞凋亡，是一種具有潛力的抗葡萄膜黑色素瘤新藥，值得進一步研究。

Uveal melanoma is the most common primary intraocular malignancy in adults and it is highly resistant to most chemotherapeutic drugs. Arsenic trioxide (ATO) has been showed to trigger apoptosis in some solid tumor cells. In present study we investigated the cytotoxic effects of ATO on human M17 uveal melanoma cell line, and explored the underlying intracellular molecular mechanisms of ATO. Using the MTT assay, we found that ATO selectively inhibited growth of uveal melanoma cells in a dose-dependent manner, and the IC50 values at 48 hr after ATO treated were 1.98±0.23 and 122.4±4.44 (g/ml for M17 and human normal fibroblast cells, respectively. After treated with 1 and 3 (g/ml of ATO for 24 hr, the apoptotic cells were increased dramatically by 18.2-and 14.5-fold in M17 cells. Furthermore, ATO treatment resulted in 4.8-, 2.8-and 4.8-fold increase in the activity of caspase-3, -8 and -9, respectively. It also increased the cytochrome c level by 2.1-fold in uveal melanoma cell. Taken together, these results suggest that ATO has a selective cytotoxic effect on human uveal melanoma cells through the caspase-activation cell apoptotic pathway.