Fumonisin B1 induces apoptosis in cultured human keratinocytes through sphinganine accumulation and ceramide depletion
Autor: | Suzanne M. Morris, Lynda J. McGarrity, Paul C. Howard, William H. Tolleson, Letha H. Couch, William B. Melchior, Levan Muskhelishvili, Olen E. Domon, M Muskhelishvili, G. R. Jenkins |
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Rok vydání: | 1999 |
Předmět: |
Keratinocytes
Cancer Research Ceramide Cell Survival Carboxylic Acids Apoptosis DNA Fragmentation Biology Ceramides Fumonisins Colony-Forming Units Assay chemistry.chemical_compound Sphingosine Fumonisin Humans Drug Interactions Enzyme Inhibitors Cells Cultured Chromatography High Pressure Liquid Fumonisin B1 Sphingolipids food and beverages Sphingolipid Cell biology Teratogens Oncology chemistry Biochemistry Epidermoid carcinoma beta-Alanine DNA fragmentation |
Zdroj: | International journal of oncology. 14(5) |
ISSN: | 1019-6439 |
Popis: | Fumonisin B1 stimulates apoptosis in a variety of cell types and tissues. We examined the role of sphingolipid changes in fumonisin B1-stimulated apoptosis. Sphinganine accumulated rapidly, sphingosine levels remained unchanged, and ceramides decreased during fumonisin B1 exposure. Increased DNA fragmentation, decreased viability, and apoptotic morphology were observed in cells exposed to fumonisin B1, sphinganine, or N-acetylsphingosine. Co-exposure to N-acetylsphingosine or beta-chloroalanine, which blocks sphinganine accumulation, partially protected cells from fumonisin B1-induced apoptosis. These results illustrate three sphingolipid-dependent mechanisms for inducing apoptosis: accumulation of excess ceramide, accumulation of excess sphinganine, and depletion of ceramide or complex sphingolipids derived from ceramide. |
Databáze: | OpenAIRE |
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