作者: Naveen Kaushal , Ujjawal H. Gandhi , Shakira M. Nelson , Vivek Narayan , K. Sandeep Prabhu
DOI: 10.1007/978-1-4614-1025-6_35
关键词: Disease 、 Proinflammatory cytokine 、 Oxidative stress 、 Cell biology 、 Immune system 、 Signal transduction 、 Selenium deficiency 、 Inflammation 、 Biology 、 Mechanism (biology)
摘要: It is becoming increasingly clear that over-production of reactive oxygen and nitrogen species (RONS) by immune cells, resulting in oxidative stress, plays a prominent role several disease states, where inflammation forms the underlying basis. Emerging evidence from many studies humans animals strongly suggest beneficial effects selenium-supplementation prevention and/or treatment some these diseases occur via mitigation inflammatory signaling pathways. Selenium supplementation, over minimal nutritional requirements, has gained popularity there scientific to support benefits super-supplementation Se. However, despite therapeutic potential selenium diseases, very little known about mechanism regulation To explain health define its biochemical mitigating stress-mediated expression proinflammatory genes initiate recovery or resolution phase, it important identify those pathways whose regulated strictly status macrophages. Given RONS serves as double-edged sword modulation pathways, not surprising find selenium-deficiency defects may be related an “over-worked” system fails mitigate stress. Thus, relating gene open new opportunities understand redox-regulation complex signal transduction