Nitric oxide (NO•) is an important signaling molecule with multiple pivotal roles in the neural and cardiovascular systems as well as in the inflammatory responses. NO• is a free short-lived radical (half-life < 0.1 s in human circulation). This unique feature makes the direct measurement of NO• almost impossible in living organisms. Many different storage forms of NO• have been suggested, including S-nitrosothiols (RSNOs) and nitrite. Oxidative stress, the imbalance between the production of reactive oxygen species (ROS) and the antioxidative defenses, is related with numerous diseases, along with some specific conditions such as hyperoxia and physical exercise. The direct damaging result of oxidative stress is the oxidation of lipids, proteins, and DNA, all of which endanger cell homeostasis. Oxidative stress also reduces NO• bioavailability. This is because ROS, notably superoxide anion (O₂^-•), oxidize NO• to peroxynitrite (ONOO^-). Furthermore, oxidative stress may cause uncoupling of the endothelial nitric oxide synthase (eNOS), thus aggravating oxidative stress. Therefore, the pro-oxidative and antioxidative states in cells and tissues determine decisively the fate and activity of NO•, RSNO, and nitrite in different conditions and in health and disease. The aim of this special issue is to assemble current information from studies performed in cell systems in vitro, as well as in animal and human studies, in the field of NO• biology and pharmacology.

We invite investigators to contribute original research articles as well as review articles that address the current standing and the progress in the area of oxidative stress in relation to NO•, its implication in disease, and the effect of the antioxidant treatment on NO•-related dysfunction. Last but not least, this special issue also aims at summarizing the current models and mechanisms of oxidative stress involving NO• and new ideas and concepts to better understand the complex and challenging nature of oxidative stress. Delineating mechanisms are essential to effectively prevent oxidative stress and to specifically improve intra- and extracellular redox status, i.e., where really required, without affecting NO•-unrelated pathways. Potential topics include, but are not limited to:

• Recent advances on the impact of oxidative stress on NO• biology
• Experimental models and molecular mechanisms of NO• lifecycle
• Effects of antioxidants against oxidative stress-induced alterations of NO• homeostasis
• Currents strategies to improve NO• bioavailability in different diseases and conditions
• Role of NO• and NO• synthase in neuronal, endothelial, and other types of cell
• Mechanisms of synthesis, metabolism, and elimination and roles of endogenous NOS inhibitors in health and disease
• Role of NO• storage forms including S-nitrosothiols and nitrite in health and disease
• Analytical methods to quantify NO•-related biomarkers of oxidative stress

Before submission, authors should carefully read over the journal’s Author Guidelines, which are located at http://www.hindawi.com/journals/omcl/guidelines/. Prospective authors should submit an electronic copy of their complete manuscript through the journal Manuscript Tracking System at http://mts.hindawi.com/submit/journals/omcl/nitox/ according to the following timetable: