目的 ·从代谢组学的角度揭示三氧化二砷（ arsenic trioxide，ATO）对肝细胞癌（ hepatocellular carcinoma，HCC）的作用机制。方法 ·分别取 ATO处理 12、24和 36 h的肝细胞癌 HepG2细胞系，通过气相色谱 /质谱联用和液相色谱 /串联质谱联用对其代谢物谱进行全局性分析。结果 ·共检测到 307种代谢物。生物信息学分析表明，糖基化和单碳代谢是主要受影响的细胞功能。其他细胞功能或途径如线粒体脂肪酸 β-氧化、三羧酸循环、戊糖磷酸途径和谷胱甘肽代谢等也受到影响。结论 · ATO通过影响 HepG2细胞主要的代谢途径，抑制细胞生长和迁移，并加剧氧化应激来诱导癌细胞凋亡。

Objective · To reveal the mechanism of the effect of arsenic trioxide (ATO) on hepatocellular carcinoma (HCC) cells through metabolomics study. Methods · HCC cell line HepG2 was treated with ATO for 12 h, 24 h and 36 h respectively. The global metabolite profiles were monitoredmetabolomics analysis using GC/MS and LC/MS/MS. Results · A total of 307 certified metabolites were detected. Bioinformatics analysis showed that glycosylation and one-carbon metabolism were the main cellular functions that have been affected. Other affected cellular functions/pathways included mitochondrial function fatty acid β-oxidation, TCA cycle, pentose phosphate pathway (PPP) and glutathione metabolism. Conclusion · ATO treatment affects the main metabolomic pathway of HepG2, and inhibits cell growth and migration, then exacerbates oxidative stress to induce cancer cell apoptosis.