Abstract
This work is dedicated to the mechanism of the antitumor action of dinitrosyl iron complexes, which generate nitric oxide NO and nitrosonium cations, NO+. The effect of diethyldithiocarbamate, used in spin trap** of NO radicals, on the antitumor activity of binuclear dinitrosyl iron complexes with glutathione or N-acetyl cysteine has been studied. The effectiveness of these drugs in vivo against solid tumors in mice persists, as expected, or even increases when they are used in combination with diethyldithiocarbamate. It is assumed that the tumor growth inhibitory effect of dinitrosyl iron complexes is due mainly to the presence of nitrosonium cations rather than the nitric oxide molecules released from dinitrosyl iron complexes.
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Abbreviations: DNIC, dinitrosyl iron complex; DETC, sodium diethyldithiocarbamate; B-DNIC-GSH, binuclear dinitrosyl iron complex with glutathione; MNIC-DETC, mononitrosyl iron complex with diethyldithiocarbamate; B-DNIC-NAC, binuclear dinitrosyl iron complex with N-acetylcysteine; i/v, intravenous(ly); i/p, intraperitoneal(ly); s/c, subcutaneous(ly).
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Vanin, A.F., Ostrovskaya, L.A., Korman, D.B. et al. Role of the Nitrosonium Cation in the Mechanism Underlying the Antitumor Effects of Drugs in Combination with Dinitrosyl Iron Complexes. BIOPHYSICS 67, 796–801 (2022). https://doi.org/10.1134/S0006350922050219
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DOI: https://doi.org/10.1134/S0006350922050219