Selenium and inflammation

Abstract

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 in several disease states, where inflammation forms the underlying basis. Emerging evidence from many studies in humans and animals strongly suggest that the beneficial effects of selenium - supplementation in prevention and/or treatment of some of these diseases occur via the mitigation of inflammatory signaling pathways. Selenium supplementation, over the minimal nutritional requirements, has gained popularity and there is some scientific evidence to support benefits of super-supplementation of Se. However, despite the therapeutic potential of selenium in many inflammatory diseases, very little is known about the mechanism and regulation of inflammation by Se. To explain the health benefits of selenium and define its biochemical role in mitigating oxidative stress-mediated expression of proinflammatory genes and initiate the recovery or resolution phase, it is important to identify those signaling pathways and genes whose expression is regulated strictly by selenium status in macrophages. Given that RONS serves as a double-edged sword in the modulation of inflammatory signaling pathways, it is not surprising to find that selenium-deficiency defects may be related to an over-worked system that fails to mitigate oxidative stress. Thus, studies relating to the modulation of signaling of inflammatory gene expression by selenium may open new opportunities to understand the redox-regulation of complex signal transduction pathways.