Nitric oxide (NO) is a key signaling molecule involved in numerous physiological and pathological processes within the human body. This review specifically examines the involvement of NO in age-related diseases, focusing on the cardiovascular, nervous, and immune systems. The discussion delves into the mechanisms of NO signaling in these diseases, emphasizing the post-translational modifications of involved proteins, such as S-nitrosation and nitration. The review also covers the dual nature of NO, highlighting both its protective and harmful effects, determined by concentration, location, and timing. Additionally, potential therapies that modulate NO signaling, including the use of NO donors and nitric oxide synthases (NOSs) inhibitors in the treatment of cardiovascular, neurodegenerative, and oncological diseases, are analyzed. Particular attention is paid to the methods for the determination of NO and its derivatives in the context of illness diagnosis and monitoring. The review underscores the complexity and dual role of NO in maintaining cellular balance and suggests areas for future research in developing new therapeutic strategies.

Exposure to environmental nanoparticles is related to the adverse impact on health, including cardiovascular system. Various forms of nanoparticles have been reported to interact with endothelium and induce inflammation. However, the potential role of nanoparticles in the pathogenesis of atherosclerosis and their mechanisms of action are still unclear. The aim of this study was to investigate the effect of two broadly used nanomaterials, which also occur in natural environment - silicon oxide (SiO₂) and ferric oxide (Fe₂O₃) in the form of nanoparticles (NPs) - on the development of atherosclerosis. We used apolipoprotein E-knockout mice exposed to silica and ferric oxide nanoparticles in a whole body inhalation chamber. Inhaled silica nanoparticles augmented the atherosclerotic lesions and increased the percentage of pro-inflammatory M1 macrophages in both the plaque and the peritoneum in apoE^-/- mice. Exposure to ferric oxide nanoparticles did not enhance atherogenesis process, however, it caused significant changes in the atherosclerotic plaque composition (elevated content of CD68-positive macrophages and enlarged necrotic core accompanied by the decreased level of M1 macrophages). Both silica and ferric oxide NPs altered the phenotype of T lymphocytes in the spleen by promoting polarization towards Th17 cells. Exposure to silica and ferric oxide nanoparticles exerts impact on atherosclerosis development and plaque composition. Pro-atherogenic abilities of silica nanoparticles are associated with activation of pro-inflammatory macrophages.

This review covers highlights of the work performed in the van Eldik group on inorganic reaction mechanisms over the past two decades in the form of a personal journey. Topics that are covered include, from NO to HNO chemistry, peroxide activation in model porphyrin and enzymatic systems, the wonder-world of Ru^III(edta) chemistry, redox chemistry of Ru(III) complexes, Ru(II) polypyridyl complexes and their application, relevant physicochemical properties and reaction mechanisms in ionic liquids, and mechanistic insight from computational chemistry. In each of these sections, typical examples of mechanistic studies are presented in reference to related work reported in the literature.

Cobalt and manganese porphyrins are known for their ability to activate small molecules. This is particularly important in the case of nitric oxide, whose role and mechanism of action in the redox biological systems have not yet been fully recognized. The goal of this article is to draw attention to some of the current trends of research in this area. The interactions involving NO itself and the primary products of its oxidation (nitrite) and reduction (nitroxyl) have been distinguished and separately discussed. The diversity of undertaken issues sheds light on both the expected behavior in biologically relevant systems as well as potential practical applications. Graphical abstract The results of recent research on interactions between cobalt and manganese porphyrins with nitric oxide species are summarized. The systems containing NO itself as well as its oxidized (nitrite) and reduced (nitroxyl) forms are discussed separately. Selected publications are primarily focused on the reaction mechanisms with respect to both biological systems and potential applications.

Despite detailed studies on nitroxylcobalamin (CblNO) formation, the possible intracellular generation of CblNO via reduction of nitrocobalamin (CblNO₂) remains questionable. To study this further, spectroscopic studies on the reaction of CblNO₂ with the intracellular antioxidant ascorbic acid (HAsc⁻) were performed in aqueous solution at pH < 5.0. It was found that nitroxylcobalamin is the final product of this interaction, which is not just a simple reaction but a rather complex chemical process. We clearly show that an excess of nitrite suppresses the formation of CblNO, from which it follows that ascorbic acid cannot reduce coordinated nitrite. We propose that under the influence of ascorbic acid, nitrocobalamin is reduced to Cbl(II) and nitric oxide (^·NO), which can subsequently react rapidly to form CblNO. It was further shown that this system requires anaerobic conditions as a result of the rapid oxidation of both Cbl(II) and CblNO. Graphical Abstract