Free Radicals and Antioxidants
Chuong Pham-Huy, Bruno Pham Huy in Food and Lifestyle in Health and Disease, 2022
Some reactive sulfur species (RSS) are thiyl radical (RS•) and peroxysulfenyl radical (RSOO•). Furthermore, some ROS such as hydrogen peroxide (H2O2), ozone (O3), singlet oxygen (1O2), lipid peroxide (LOOH), and hypochlorous acid (HOCl), are not considered free radicals, and are generally called oxidants because they are more and less stable. It is the same for some RNS like nitrous acid (HNO2), dinitrogen trioxide (N2O3), and some RSS such as sulfite (SO3 –), disulfide (DSSO), and sulfenic acid (RSOH). However, these oxidants can easily lead to free radical reactions in living organisms and can yield reactive species – active free radicals (6, 15, 17–19).
Ecology
Paul Pumpens in Single-Stranded RNA Phages, 2020
Inactivation by nitrous acid initiated the studies on the RNA phage genetics and resulted in numerous RNA phage mutants that are described in Chapter 9. Briefly, nitrous acid acted as a deamination agent on adenine, guanine, and cytosine, where adenine was converted to hypoxanthine, cytosine was converted to uracil, and guanine was converted to xanthine, which resulted in mispairing. The first nitrous acid inactivation, or mutagenesis, experiments were performed on the phages fr, or formerly ft5 (Kaudewitz and Knolle 1963), μ2 (Turri et al. 1964), and MS2 (Sherban 1969; Sherban and Krivisky 1969).
Tobacco and Health
Rajmohan Panda, Manu Raj Mathur in Tobacco Cessation, 2019
When tobacco is burning, it releases nicotine in the form of a vapor. This vapor attaches to surfaces such as walls, floors, carpeting, drapes, and furniture. Nicotine reacts with nitrous acid (one source of which is burning tobacco) and forms cancer-causing tobacco-specific nitrosamines (TSNAs). Nicotine can last for months on indoor surfaces. This means that these TSNAs are always being created. TSNAs are then inhaled, absorbed, or ingested. Anyone who smokes in any enclosed space (like a car or home) is exposing nonsmokers to TSNAs.
Electrophysiological characterization of the activating action of a novel liposomal nitric oxide carrier on Maxi-K channels in pulmonary artery smooth muscle cells
Published in Journal of Liposome Research, 2021
Irina V. Ivanova, Mariia I. Melnyk, Dariia O. Dryn, Vitalii V. Prokhorov, Alexander V. Zholos, Anatoly I. Soloviev
To remove atmospheric oxygen, a high purity argon gas was pumped for 30 min through a liposomal emulsion of cytochrome c (100 ml) obtained after homogenization. The aim of this procedure was to prevent nitrous acid formation due to NO reaction with oxygen in the aqueous medium. After that, NO obtained in the reaction of nitric acid and metallic copper was fed into the emulsion in an argon flow. The mixture of gases was first passed through a solution of sodium hydroxide to remove the salt-forming oxides. Simultaneously, the liposome emulsion was acidified with nitric acid to pH 6.3–6.5. In this case, the liposomal cytochrome c was transformed into a reduced form (cytc3+ –NO). The transition indicator was a change in the colour of the emulsion from reddish-brown to bright pink, as well as spectral absorption peaks at 528 nm and 560 nm. To stabilize the liposomal cytochrome c, 10 mg of GSNO was added to the emulsion.
S-Nitrosoglutathione formation at gastric pH is augmented by ascorbic acid and by the antioxidant vitamin complex, Resiston
Published in Pharmaceutical Biology, 2018
Vitali I. Stsiapura, Ilya Bederman, Ivan I. Stepuro, Tatiana S. Morozkina, Stephen J. Lewis, Laura Smith, Benjamin Gaston, Nadzeya Marozkina
Our data suggest that the increased GSNO formation at pH range of 2.5–4.5 in the presence of ascorbate could most likely be explained by O-nitrosoascorbic acid formation that serves as a donor–acceptor for NO+ (Figure 7). The AA does not appear to act through reduction of oxidized thiol (Figure 4). With regard to the possibility that GSNO could be formed in the stomach, our data confirm that GSNO is formed from physiological levels of GSH and nitrite in the aqueous solutions at different pH and in human gastric fluid. Reaction of nitrous acid HNO2 with GSH is responsible for the GSNO formation and its rate increases with lower pH due to the protonation of nitrite ion:
Urinary sulphated glycosaminoglycans excretion in obese patients with type 2 diabetes mellitus treated with metformin
Published in Archives of Physiology and Biochemistry, 2022
Agnieszka Jura-Półtorak, Paweł Olczyk, Aleksandra Chałas-Lipka, Katarzyna Komosińska-Vassev, Kornelia Kuźnik-Trocha, Katarzyna Winsz-Szczotka, Diana Ivanova, Yoana Kiselova-Kaneva, Katarzyna Krysik, Alicja Telega, Krystyna Olczyk
The total sulphated glycosaminoglycans were quantitated using the Blyscan™ Sulphated Glycosaminoglycan Assay kit (Biocolor Ltd., United Kingdom), based on the reaction of 1.9-dimethylmethylene blue with sulphated GAGs. For the quantitative measurement of CS/DS, isolation procedure of these glycans was performed. It consisted of removing the HS fraction from the samples received at an earlier stage, containing a total pool of urinary sulphated GAGs. Degradation of HS was performed with nitrous acid treatment. Urinary HS concentrations were quantitate as a percentage difference between sulphated GAGs concentration in urine sample with and without nitrous acid treatment.
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