ABSTRACT
This chapter reviews some of the models for redox control of gene expression, with special emphasis on nitric oxide (NO) as a signaling molecule. Although an important effect of reactive oxygen species in sepsis is to alter the redox balance of cells, reduction products of molecular oxygen are the only cause of redox stress. Nitric oxide not only acts as a weak oxidizing agent, but can provide important antioxidant functions for cells as well. Given the efficiency with which NO nitrosylates GSH, a mechanism in which nitroso-gluthathione or glutathione disulfide serves as an intermediate sensing protein may similarly explain several aspects of NO-induced redox stress. The chapter considers the negative consequences of redox stress, a certain level of cellular redox imbalance may be beneficial for controlling inflammatory mediator production.
