ABSTRACT
I. INTRODUCTION Nitric oxide (·NO) is an endogenously synthesized free radical first characterized as a component of the endothelial-derived relaxation factor (EDRF) (1,2). The physiological actions of ·NO range from mediating vasodilation and neurotransmission, inhibiting platelet adherence and aggregation, and the macrophage and neutrophil killing of pathogens (3,4). The broad distribution of sites of production of ·NO, combined with its facile reactions with metalloproteins and radical species, determines that ·NO plays an important role in regulating critical oxidant reactions. The influence of ·NO in redox and free radical processes extends beyond its recognized ability to mediate signal transduction by stimulation of guanylate cyclase-mediated cGMP synthesis (5,6). Chemical reaction systems, cell and animal models, and clinical studies have recently revealed an ability of ·NO to modulate reactions and pathological processes associated with the excess production and biological effects of reactive oxygen species (ROS). The focus of this chapter will be to analyze the antioxidant properties of ·NO in the context of the current knowledge on the target molecule reactivities of this free radical species. This biochemical foundation provides the rationale to understand many cytoprotective actions of ·NO, which are due to its ability to redirect the reactivity of partially reduced oxygen and nitrogen species and opens the possibility of pharmacological developments directed at inhibiting oxidative processes involving the delivery of ·NO.
