n-caproylsphingosine and Leukemia--T-Cell

n-caproylsphingosine has been researched along with Leukemia--T-Cell* in 1 studies

Other Studies

1 other study(ies) available for n-caproylsphingosine and Leukemia--T-Cell

Article	Year
Synthetic ceramides induce growth arrest or apoptosis by altering cellular redox status. Archives of biochemistry and biophysics, 2002, Nov-01, Volume: 407, Issue:1 Reactive oxygen species (ROS) and ceramide are each partly responsible for the signal transduction of a variety of extracellular agents. Furthermore, the application of synthetic, short-chain ceramides mimics the cellular responses to these extracellular agents. However, the significance of ROS involvement in ceramide signaling pathways is poorly understood. Here we describe that the cellular responses to C2-/C6-ceramide of growth arrest in U937 monocytes and apoptosis in Jurkat T-cells are preceded by a rise in mitochondrial peroxide production. In Jurkat T-cells, this is associated with a large time- and dose-dependent loss of cellular glutathione. However, in U937 monocytes, glutathione loss is transient. Differences in the magnitude and kinetics of this alteration in cellular redox state associate with discrete outcomes, namely growth arrest or apoptosis. Topics: Apoptosis; Buthionine Sulfoximine; Cell Division; Cells, Cultured; Ceramides; Dose-Response Relationship, Drug; Glutathione; Humans; Jurkat Cells; Leukemia, T-Cell; Mitochondria; Monocytes; Oxidation-Reduction; Peroxides; Reactive Oxygen Species; Rotenone; Sphingosine	2002

Article

Year

Synthetic ceramides induce growth arrest or apoptosis by altering cellular redox status.

Archives of biochemistry and biophysics, 2002, Nov-01, Volume: 407, Issue:1

Reactive oxygen species (ROS) and ceramide are each partly responsible for the signal transduction of a variety of extracellular agents. Furthermore, the application of synthetic, short-chain ceramides mimics the cellular responses to these extracellular agents. However, the significance of ROS involvement in ceramide signaling pathways is poorly understood. Here we describe that the cellular responses to C2-/C6-ceramide of growth arrest in U937 monocytes and apoptosis in Jurkat T-cells are preceded by a rise in mitochondrial peroxide production. In Jurkat T-cells, this is associated with a large time- and dose-dependent loss of cellular glutathione. However, in U937 monocytes, glutathione loss is transient. Differences in the magnitude and kinetics of this alteration in cellular redox state associate with discrete outcomes, namely growth arrest or apoptosis.

Topics: Apoptosis; Buthionine Sulfoximine; Cell Division; Cells, Cultured; Ceramides; Dose-Response Relationship, Drug; Glutathione; Humans; Jurkat Cells; Leukemia, T-Cell; Mitochondria; Monocytes; Oxidation-Reduction; Peroxides; Reactive Oxygen Species; Rotenone; Sphingosine

2002