[Dinitrosyl iron complexes reacts with diethyldithiocarbamate in the blood of anesthetized rats: specific physico-chemical and physiological characteristics of the products].

Diethyldithiocarbamate (DETC) attenuated sharply the hypotensive effect of dinitrosyl iron complexes (DNIC) with cysteine or phosphate anions being injected into rats simultaneously with DNICs or 10 min after them. This addition of DETC accelerated the restoration of blood pressure to the initial level in the animals which was diminished with DNIC injection. EPR analysis showed the disappearance of protein DNIC which were initially formed in blood plasma or in the liver tissue of rats treated with low molecular DNICs, and the appearance of mononitrosyl iron complexes with DETC (MNIC-DETC). The latters were located in a blood cells but also disappeared after 30-40 min. Protein DNICs appeared in blood cells instead of MNIC-DETC, which were characterized with a specifically shape of their EPR signal. The amplitude of peak at g[symbol: see text] 11 was smaller for this signal as compared with that for DNIC with cysteine. The transformation of MNIC-DETC into this DNIC did not occur in a blood cells of rats treated with sodium nitroprusside and DETC. MNIC-DETC was only observed in blood cells of these animals: the disapperance of these complexes was not followed with DNIC formation in blood cells. The formation of a nitrosocompounds was proposed as a result of DNIC reaction with DETC. This reaction provided the transfer of Fe(+)-NO+ groups from DNIC to DETC. Second NO molecule released from DNIC as a NO+ group attacks various chemical groups resulted in a nitrosocompound formation. The following decomposition of these nitrosocompounds provided specifically DNIC formation in blood cells.