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.
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