OBJECTIVE: Cytokines, nitric oxide (NO) and reactive oxygen species (ROS) are well known for their pathogenic effects in development of cardiovascular diseases. Interleukin-1beta (IL-1beta) is known to induce NO generation, however it is not well established if IL-1beta or NO regulate production of ROS, such as superoxide anion. Therefore, the main objective of this study was to evaluate the effect of IL-1beta or NO on enzyme activity of NADPH oxidase (NOX), a superoxide-generating system recently documented to participate in a variety of vascular functions. METHODS: Human coronary artery smooth muscle cells (SMC) obtained from Clonetics were treated with IL-1beta and NO donor, sodium nitroprusside (SNP), in culture. Nitrites accumulated in supernatants of SMC cultures were measured as an index of NO released following treatment with IL-1beta. NOX enzyme activity was assayed using cytochrome c as the electron acceptor. RESULTS: Treatment with IL-1beta resulted in a 3-fold increase in the production of NO by SMC. Both IL-1beta and SNP enhanced NOX activity, by 67 and 45%, respectively, following 24 h of treatment. CONCLUSION: This study suggests that NO or NO- generating cytokines might regulate the production of ROS in the cardiovascular system through modulation of superoxide-generating systems such as NOX. Copyright 2004 S. Karger AG, Basel
OBJECTIVE: Cytokines, nitric oxide (NO) and reactive oxygen species (ROS) are well known for their pathogenic effects in development of cardiovascular diseases. Interleukin-1beta (IL-1beta) is known to induce NO generation, however it is not well established if IL-1beta or NO regulate production of ROS, such as superoxide anion. Therefore, the main objective of this study was to evaluate the effect of IL-1beta or NO on enzyme activity of NADPH oxidase (NOX), a superoxide-generating system recently documented to participate in a variety of vascular functions. METHODS:Human coronary artery smooth muscle cells (SMC) obtained from Clonetics were treated with IL-1beta and NO donor, sodium nitroprusside (SNP), in culture. Nitrites accumulated in supernatants of SMC cultures were measured as an index of NO released following treatment with IL-1beta. NOX enzyme activity was assayed using cytochrome c as the electron acceptor. RESULTS: Treatment with IL-1beta resulted in a 3-fold increase in the production of NO by SMC. Both IL-1beta and SNP enhanced NOX activity, by 67 and 45%, respectively, following 24 h of treatment. CONCLUSION: This study suggests that NO or NO- generating cytokines might regulate the production of ROS in the cardiovascular system through modulation of superoxide-generating systems such as NOX. Copyright 2004 S. Karger AG, Basel
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