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The Biological Effect of Dinitrosyl Iron Complexes with Glutathione upon Nitric Oxide Hyperproduction Induced by Endotoxin Shock

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Abstract—The objective of this work was to study the biological effect of dinitrosyl iron complexes (DNICs) with the glutathione ligand (GSH−DNICs) as a stabilized form of nitric oxide in a rat model of nitric oxide hyperproduction induced by inflammation. Administration of GSH−DNICs in endotoxin shock did not increase the total nitric oxide levels in rat organs, but exerted a protective effect by suppressing nitric oxide hyperproduction in the liver and led to an accumulation of the complexes with protein ligands in the kidney.

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Funding

This work was supported by the Russian Foundation for Basic Research (project no. 18-015-00027).

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Correspondence to A. A. Timoshin.

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Conflict of interests. The authors declare that they have no conflict of interest.

Statement on the welfare of animals. All applicable international, national, and/or institutional guidelines for the care and use of animals were followed.

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Translated by T. Tkacheva

Abbreviations: DNIC, dinitrosyl iron complex; GSH−DNICs, dinitrosyl iron complex with glutathione as a ligand; LPS, lipopolysaccharide; AST, aspartate aminotransferase; EPR, electron paramagnetic resonance.

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Timoshin, A.A., Lakomkin, V.L., Abramov, A.A. et al. The Biological Effect of Dinitrosyl Iron Complexes with Glutathione upon Nitric Oxide Hyperproduction Induced by Endotoxin Shock. BIOPHYSICS 64, 89–94 (2019). https://doi.org/10.1134/S0006350919010196

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  • DOI: https://doi.org/10.1134/S0006350919010196

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