Antimicrobial properties of diethylamine NONOate, a nitric oxide donor, against Escherichia coli: a pilot study

Sysel, Annette M.; Dunphy, Michael; Bauer, Joseph A.

doi:10.1038/s41429-020-00397-9

Cited by 10 publications

(5 citation statements)

References 66 publications

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“…NO-releasing molecules have shown potential applications as antibacterial, antiviral, and antitumor agents. , The diseases caused by bacterial infections have become a concern to health as many bacterial micro-organisms have become resistant to antibiotics. Antibacterial resistance has been recognized as a global threat to human health.…”

Section: Resultsmentioning

confidence: 99%

Regulation of Nitric Oxide (NO) Release by Membrane Fluidity in Ruthenium Nitrosyl Complex-Embedded Phospholipid Vesicles

et al. 2022

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Incorporating water-insoluble nitric oxide (NO)-releasing molecules into biocompatible vesicles may allow for the tunable control of NO release on a specific target site. In vesicles, membrane fluidity plays an important role and influences the final therapeutic efficiency of drugs loaded into the vesicles. Hence, we aimed to investigate the effect of lipid fluidity on the NO release behavior of the photo-controllable ruthenium nitrosyl (Ru-NO) complex. In this regard, a new photoactive ruthenium nitrosyl complex (L.Ru-NO) with amphiphilic terpyridine ligand was synthesized and characterized in detail. L.Ru-NO was incorporated with commercial phospholipids to form nanoscale vesicles L.Ru-NO@Lip. The photoactive {Ru-NO}6 type complex released NO in the organic solvent CH3CN and aqueous liposome solution by irradiating under low-intensity blue light (λ = 410 nm, 3 W). To demonstrate the effect of lipid structure and fluidity on NO release, four different liposome systems L.Ru-NO@Lip1–4 were prepared by using phospholipids such as DOPC, DSPC, DPPC, and DMPC having different chain lengths and saturation. The NO-releasing abilities of these liposomes in aqueous medium were studied by UV–vis spectrum, colorimetric Greiss, and fluorescent DAF assay. The results show that the rate of NO release could be easily tuned by varying the lipid fluidity. The effect of temperature and pH on NO release was also studied. Further, the complex L.Ru-NO and liposomes L.Ru-NO@Lip1 were assayed as an antibacterial agent against the strains of bacteria Escherichia coli and Staphylococcus aureus.

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Section: Resultsmentioning

confidence: 99%

Regulation of Nitric Oxide (NO) Release by Membrane Fluidity in Ruthenium Nitrosyl Complex-Embedded Phospholipid Vesicles

et al. 2022

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“…-Nitrates (such as nitroglycerin, sodium nitroprusside, nitrosorbide, commonly used in the clinic) [270][271][272][273][274], -Nitrites (amyl nitrite, NaNO2), -Nitrosothiols and substances that form various complexes with NO: S-nitrosoglutathione (GSNO), S-nitroso-N-acetylpenicillamine (SNAP), diethylamine-NO (DEA-NO).…”

Section: Exogenous Nitric Oxidementioning

confidence: 99%

Nitric Oxide in the Mechanisms of Cell Death and Cytoprotection

Belenichev,

Popazova,

Bukhtiyarova

et al. 2024

Preprint

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The regulation of cell death is a fundamental issue in cell biology and continues to be intensely investigated worldwide. The significance of research in this field persists because understanding the determinants of cell lifespan directly impacts the maintenance of multicellular organism homeostasis and, consequently, is crucial for addressing biomedical challenges associated with various diseases. It is recognized that the initiation of cell death can be prompted by both specific signals (such as cytokines or hormones) and nonspecific stimuli, including radiation, temperature increase, or oxidants. When these factors affect a cell, numerous signaling pathways are triggered in the cell, leading to neutralization of the effects of their negative effects or, in case of irreparable damage, to cell elimination. This removal of damaged cells occurs through apoptosis or programmed cell death, a highly regulated process. Numerous signaling molecules participate in orchestrating the apoptotic process, many of which also govern other essential functions within the organism. Physiological factors capable of triggering the apoptotic program in cells include nitric oxide (NO), which serves as one of the key signaling molecules regulating the functions of the cardiovascular, nervous, and immune systems of the organism. The unique chemical nature of NO, along with its numerous intracellular targets and physiologically active redox forms, raises questions about the specific mechanisms through which NO exerts its damaging effects on cells. Utilizing pharmacological preparations- such as sources (donors) of exogenous nitric oxide- represents an approach to investigating the initiation and execution of the apoptotic program in sensitive target cells. Furthermore, this approach holds promise as a direction for discovering new selective drugs.

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“…-Nitrates (such as nitroglycerin, sodium nitroprusside, and nitrosorbide, commonly used in the clinic) [268][269][270][271][272], -Nitrites (amyl nitrite, NaNO 2 ), -Nitrosothiols and substances that form various complexes with • NO: S-nitrosoglutathione (GSNO), S-nitroso-N-acetylpenicillamine (SNAP), diethylamine-NO (DEA-NO).…”

Section: Exogenous • Nomentioning

confidence: 99%

Modulating Nitric Oxide: Implications for Cytotoxicity and Cytoprotection

Belenichev,

Popazova,

Bukhtiyarova

et al. 2024

Antioxidants

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Despite the significant progress in the fields of biology, physiology, molecular medicine, and pharmacology; the designation of the properties of nitrogen monoxide in the regulation of life-supporting functions of the organism; and numerous works devoted to this molecule, there are still many open questions in this field. It is widely accepted that nitric oxide (•NO) is a unique molecule that, despite its extremely simple structure, has a wide range of functions in the body, including the cardiovascular system, the central nervous system (CNS), reproduction, the endocrine system, respiration, digestion, etc. Here, we systematize the properties of •NO, contributing in conditions of physiological norms, as well as in various pathological processes, to the mechanisms of cytoprotection and cytodestruction. Current experimental and clinical studies are contradictory in describing the role of •NO in the pathogenesis of many diseases of the cardiovascular system and CNS. We describe the mechanisms of cytoprotective action of •NO associated with the regulation of the expression of antiapoptotic and chaperone proteins and the regulation of mitochondrial function. The most prominent mechanisms of cytodestruction—the initiation of nitrosative and oxidative stresses, the production of reactive oxygen and nitrogen species, and participation in apoptosis and mitosis. The role of •NO in the formation of endothelial and mitochondrial dysfunction is also considered. Moreover, we focus on the various ways of pharmacological modulation in the nitroxidergic system that allow for a decrease in the cytodestructive mechanisms of •NO and increase cytoprotective ones.

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Antimicrobial properties of diethylamine NONOate, a nitric oxide donor, against Escherichia coli: a pilot study

Cited by 10 publications

References 66 publications

Regulation of Nitric Oxide (NO) Release by Membrane Fluidity in Ruthenium Nitrosyl Complex-Embedded Phospholipid Vesicles

Regulation of Nitric Oxide (NO) Release by Membrane Fluidity in Ruthenium Nitrosyl Complex-Embedded Phospholipid Vesicles

Nitric Oxide in the Mechanisms of Cell Death and Cytoprotection

Modulating Nitric Oxide: Implications for Cytotoxicity and Cytoprotection

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