title: Effect of purified allicin, the major ingredient of freshly crushed garlic, on cancer cell proliferation.
abstract: The diverse health benefit effects of garlic include its anticancer activity. However, very little is known about such activity of isolated garlic compounds, among which allicin (the major ingredient of crushed garlic) has been the least studied. The aim of this work was to determine whether pure allicin exhibits the antiproliferative effect reported for garlic in in vitro models. Allicin, but not its precursor alliin, inhibited proliferation of human mammary (MCF-7), endometrial (Ishikawa), and colon (HT-29) cancer cells (50% inhibitory concentration = 10-25 microM). Two of three tested primary lines of human fibroblasts displayed a similar response to allicin (50% inhibitory concentration = 16-40 microM), whereas the third line was almost unaffected by this compound. The pure allicin and water extract of garlic powder with equivalent allicin concentrations displayed a similar potency, suggesting that allicin is responsible for the antiproliferative effect of the extract. The growth inhibition was accompanied by accumulation of cells in the G0/G1 and G2/M phases of the cell cycle (MCF-7 cells) and not by a significant increase in cell death. Allicin caused a transient drop in the intracellular glutathione (GSH) level, the magnitude and kinetics of which significantly varied depending on cell type. The extent of the decrease in GSH levels correlated well (r = 0.75) with the growth inhibitory activity of allicin. On the basis of these findings, we suggest that allicin plays a major role in the antiproliferative effect of water-soluble garlic preparations and that this effect may be attributed to the ability of allicin to transiently deplete the intracellular GSH level.
authors.affiliation: Department of Clinical Biochemistry, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel.
authors.forename: K
authors.initials: K
authors.lastname: Hirsch
authors.forename: M
authors.initials: M
authors.lastname: Danilenko
authors.forename: J
authors.initials: J
authors.lastname: Giat
authors.forename: T
authors.initials: T
authors.lastname: Miron
authors.forename: A
authors.initials: A
authors.lastname: Rabinkov
authors.forename: M
authors.initials: M
authors.lastname: Wilchek
authors.forename: D
authors.initials: D
authors.lastname: Mirelman
authors.forename: J
authors.initials: J
authors.lastname: Levy
authors.forename: Y
authors.initials: Y
authors.lastname: Sharoni
mesh_terms: D000972:Antineoplastic Agents, Phytogenic / Q000494:pharmacology*; D002453:Cell Cycle / Q000187:drug effects; D016923:Cell Death / Q000187:drug effects; D002455:Cell Division / Q000187:drug effects; D002471:Cell Transformation, Neoplastic / Q000187:drug effects*; D003110:Colonic Neoplasms / Q000473:pathology; D004220:Disulfides; D004305:Dose-Response Relationship, Drug; D016889:Endometrial Neoplasms / Q000473:pathology; D005260:Female; D005347:Fibroblasts / Q000166:cytology / Q000187:drug effects; D005737:Garlic / Q000737:chemistry*; D005978:Glutathione / Q000378:metabolism; D006801:Humans; D007700:Kinetics; D008297:Male; D015674:Mammary Neoplasms, Animal / Q000473:pathology; D010936:Plant Extracts; D010946:Plants, Medicinal; D013441:Sulfinic Acids / Q000494:pharmacology*; D014407:Tumor Cells, Cultured
chemical_list: D000972:Antineoplastic Agents, Phytogenic; D004220:Disulfides; D010936:Plant Extracts; D013441:Sulfinic Acids; C006452:allicin; D005978:Glutathione