Wu C.-C.Chung J.G.Tsai S.-J.Yang J.H.Sheen L.Y.2019-07-112019-07-1120042786915https://scholars.lib.ntu.edu.tw/handle/123456789/413589In this study, diallyl sulfide (DAS), diallyl disulfide (DADS) and diallyl trisulfide (DATS), which are major organosulfur compounds (OSCs) of garlic, were used as experimental materials to investigate their modulation effects on cell viability and cell cycle in human liver tumor cells (J5). According to the results of cell viability assay, 50 or 100 £gM DATS significantly decreased the cell viability as compared with the control (P < 0.05) in dose and time dependent relations. Phenomena of cell number loss, shape deformation and lysis were observed after treatment with 100 £gM DATS for 24 h. Cell cycle studies showed that J5 cells were significantly arrested in G2/M phase as the cells were treated with 100 £gM DADS, 10, 50 or 100 £gM DATS for 24 h (P < 0.05). DATS was more effective in arresting cells in G2/M phase than DADS, and the phenomena of arresting J5 cells in G2/M phase increased obviously in dose and time dependent relations. According to the Western blot analysis, DATS decreased cyclin-dependent kinase (Cdks)-Cdk7 (i.e. Cdc2 activate kinase) protein levels in J5 cells but increased cyclin B1 protein level. The modulation potency to cyclin B1 and Cdk7 expressions was in the order of DATS > DADS > DAS. The modulation potency to cyclin B1 and Cdk7 protein levels increased with increasing in DATS concentration and culture time. In conclusion, DATS might affect cell viability and cell morphological changes in J5 cells and lead cells to be arrested in G2/M phase via controlling the expression of cyclin B1 and Cdk7 in J5 cells, and the controlling action might relate to the sulfuric atom numbers in the structures of all these allyl sulfides. ? 2004 Elsevier Ltd. All rights reserved.Cell cycleDiallyl disulfideDiallyl sulfideDiallyl trisulfideGarlicHuman liver tumor cellsjournal article10.1016/j.fct.2004.07.0082-s2.0-7044263002https://www.scopus.com/inward/record.uri?eid=2-s2.0-7044263002&doi=10.1016%2fj.fct.2004.07.008&partnerID=40&md5=f4efac618d25f962230ded1ee211a83a