There is an emerging concept that nitric oxide (NO), its derivatives and reactive oxygen intermediates (ROS) are the major determinants of the involvement of oxidant stress that contributes to the control of physiological cell signalling processes, blood flow regulation and pathological hypoxia. There is recent published evidence for additional functions of these oxygen metabolites in cardiac gene expression; functions that include the modulation of the cytokine response of lymphocytes and the regulation of immune cell apoptosis as well as immuno-deviating effects. In vitro and in vivo experimental models investigating the biological nature of ROS have shown that there is a concentration dependent effect of NO and that differences in cell sensitivity to NO may have an impact upon the degree of immune or inflammatory state. Disturbances in NO bio-availability leads to loss of cardioprotective actions within biological systems and in some cases may even increase oxidative stress and disease progression. Hence, considerable interest in identifying the mechanisms involved in their generation and implications have spurted in the hope that inhibition strategies can be developed either bio-materially or pharmacologically. This book brings together the emerging biological concepts of oxidative stress and its connotation in the pathogenesis of various inflammatory processes in biological systems.