Abstract
Reactive oxygen species (ROS) are produced in all mammalian cells as a result of normal cellular metabolism and due to the activation of oxidant-producing enzymes in response to exogenous stimuli. The balance between ROS production and antioxidant defenses determines the degree of oxidative stress. Generation of ROS has been associated with cell signaling, stress responses, cell proliferation, aging and cancer development. The ability of ROS to induce cellular damage and to cause cell death opens the possibility to exploit this property in the treatment of cancer through a free radical-mediated mechanism.
Keywords: ros, b cells, lymphoproliferative disorders, rituximab, 2-methoxyoestradiol, imexon, arsenic trioxide 1, 4- benzodiazepine
Current Pharmaceutical Design
Title: Cytotoxic Effects on B Lymphocytes Mediated by Reactive Oxygen Species
Volume: 10 Issue: 8
Author(s): Neus Villamor, Emili Montserrat and Dolors Colomer
Affiliation:
Keywords: ros, b cells, lymphoproliferative disorders, rituximab, 2-methoxyoestradiol, imexon, arsenic trioxide 1, 4- benzodiazepine
Abstract: Reactive oxygen species (ROS) are produced in all mammalian cells as a result of normal cellular metabolism and due to the activation of oxidant-producing enzymes in response to exogenous stimuli. The balance between ROS production and antioxidant defenses determines the degree of oxidative stress. Generation of ROS has been associated with cell signaling, stress responses, cell proliferation, aging and cancer development. The ability of ROS to induce cellular damage and to cause cell death opens the possibility to exploit this property in the treatment of cancer through a free radical-mediated mechanism.
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Cite this article as:
Villamor Neus, Montserrat Emili and Colomer Dolors, Cytotoxic Effects on B Lymphocytes Mediated by Reactive Oxygen Species, Current Pharmaceutical Design 2004; 10 (8) . https://dx.doi.org/10.2174/1381612043452848
DOI https://dx.doi.org/10.2174/1381612043452848 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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