Please use this identifier to cite or link to this item: https://scidar.kg.ac.rs/handle/123456789/11886
Title: Protective role of carbon dioxide (CO<inf>2</inf>) in generation of reactive oxygen species
Authors: Bolevich, Sergey
KOGAN A.
Zivkovic V.
Djuric D.
Novikov, Alexei Alekseevich
Vorobyev, Sergey
Jakovljevic V.
Journal: Molecular and Cellular Biochemistry
Issue Date: 1-Jan-2016
Abstract: © 2015, Springer Science+Business Media New York. The results testify to the fact that CO2 is a powerful inhibitor of reactive oxygen species (ROS) generation by cells (blood phagocytes and alveolar macrophages of 96 people and cells of inner organs and tissue phagocytes (of liver, brain, myocardium, lungs, kidneys, stomach, and skeleton muscles), as well as by mitochondria of the liver of 186 white mice and human tissues. Generation of ROS was determined using various methods with CO2 directly acting on the cells and bioptates and indirectly on the organism as a whole. CO2 in the concentration of 5.1 % (P = 37.5 mmHg), 8.2 % (P = 60.0 mmHg), and 20 % (P = 146.0 mmHg) in a mixture with air (total pressure = 730 mmHg) inhibits the basal ROS generation by phagocytes on the average by 3.52, 5.69, and 10.03 times, respectively (p < 0.05), and the stimulated by corpuscular particles: (a) zymosan by 3.24, 4.43, and 7.95 times; (b)SiO2: by 2.99, 3.24, and 5.76 times (p < 0.05). This is confirmed by the feet that CO2, along with inhibiting the O2− generation by cells of the various organs, including the liver, as a rule, by 2.19–4.7 times, p < 0.01 or <0.001 induces simultaneously a decrease in the O2− generation by mitochondria isolated from the liver (by 1.91–3.2 times, p < 0.001). The mechanism of CO2 influence is realized, in part, by inhibition of NADPH-oxidase activity. Taken into consideration proven role of CO2 in different pathophysiological conditions, (such as endoarteritis, bronchial asthma, and infectious diseases), present findings may be of clinical interest in terms of potential implementation of CO2 donors as adjuvant therapeutics in these diseases.
URI: https://scidar.kg.ac.rs/handle/123456789/11886
Type: journal article
DOI: 10.1007/s11010-015-2594-9
ISSN: 03008177
SCOPUS: 84957434842
Appears in Collections:University Library, Kragujevac

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