[The effect of ionizing radiation at superhigh doses on the processes of dopamine release and reuptake by nerve endings in different sections of the brain]. / Vliianie ioniziruiushchego izlucheniia v sverkhvysokikh dozakh na protsessy vysvobozhdeniia i obratnogo zakhvata dofamina nervnymi terminaliami razlichnykh otdelov golovnogo mozga.

Rats exposed to fast 24 MeV electrons (100 Gy) at the state of early transient incapacity (ETI) exhibited active release and reuptake of dopamine in nerve terminals of the striatum. No changes in the indices under study were found in rats exposed to 25 Gy radiation that did not cause the ETI development. The in vitro irradiation of the isolated synaptosomes (100 Gy) inhibited dopamine reuptake and increased the number of sites of 3H-spiperone binding to D2-receptors in a membrane fraction isolated from the striatum.

[Biochemical reception and ionizing irradiation of the body]. / Biokhimicheskaia retseptsiia i ioniziruiushchee obluchenie organizma.

The authors present the idea of the importance of studying the mechanism of biochemical reception of biologically active compounds (BAC) particularly the reception of prostaglandins after the effect of ionizing radiation on eucaryotes as a factor playing a significant role in understanding the radiation sickness pathogenesis. The perspectives of studying BAC reception are prognosticated for searching new radiomodifying agents (radioprotectors and means for treating radiation sickness).

[Prostaglandins and interphase death of irradiated cells]. / Prostaglandiny i interfaznaia gibel' obluchennykh kletok.

The contribution of the post-irradiation changes in prostaglandin transformation to the biochemical mechanism of interphase death of irradiated cells is estimated. It is supposed that prostaglandins are secondary trigger-effectors which initiate the development of primary biochemical reactions giving rise to radiation sickness. It is suggested that the biochemical mechanism of interphase death is complex and involves several concurrent trigger mechanisms including prostaglandin regulation system.

[Effect of different doses of ionizing radiation on the binding of prostaglandin E2 in mouse tissues]. / Deistvie ioniziruiushchego izlucheniia v raznykh dozakh na sviazyvanie prostaglandina E2 v tkaniakh myshei.

The effect of various radiation doses on membrane reception of prostaglandin E2(PGE2) of spleen, small intestine, brain, and liver cells of mice was studied in dynamics. Irradiation of the animals with doses producing bone marrow, intestinal and cerebral forms of radiation sickness was shown to change specific binding of PGE2 to cell membranes of both radiosensitive tissues and a relatively radioresistant organ, the liver.

[Action of modifiers of a radiation lesion on the binding of prostaglandin E2 with liver membranes in F1 CBA X C57BL strain mice]. / Deistvie modifikatorov luchevogo porazheniia na sviazyvanie prostaglandina E2 s membranami pecheni myshei linii F1 CBA X C57BL.

Prostaglandin E2 (PGE2) was specifically bound by the membrane fraction prepared from the mouse liver. The binding constants indicate the presence of high-affinity PGE2 binding sites with an apparent dissociation constant (Kd) of 0.82 X 10(-9) M and a capacity of 0.36 X 10(9) M/mg protein and a lower affinity PGE2 binding site with Kd = 15.73 X 10(-9) M and a capacity of 5.31 X 10(9) M/mg protein. The radioprotectors, MEA and APAETP inhibit PGE2 binding and alter its kinetics. Apparently the mechanism of PGE2 binding by membranes is related to interaction of prostaglandins with thiols and sufhydryl groups of membrane lipoproteins, while the radioprotectors modify the functional groups participating in receptor PGE2 binding.

[Interaction of beta-mercaptoethylamine with the enzymatic system responsible for the biosynthesis of prostaglandins E2 and F2 alpha]. / Vzaimodeistvie beta-merkaptoétilamina s fermentnoi sistemoi, uchastvuiushchei v biosinteze prostaglandinov E2 i F2 alpha.

After intraperitoneal administration of beta-mercaptoethylamine (MEA) into mice of F1 strain (CBA XC57B1) at a radioprotective dose, activity of PGE2 and PGF2 alpha-synthetases was decreased in liver microsomes, testicular and brain supernatants (16,000xg) within 15 min, which corresponded to period of the highest radioprotector activity. Amount of newly synthesized prostaglandins was increased in liver tissue within the subsequent periods. Within 3 hrs after the radioprotector administration these amounts constituted for PGE2 246% and for PGF2 alpha 262% as compared with controls; at the same time, activity of PG-synthetases in testes was normalized. In the brain tissue within 1 hr the newly synthesized prostaglandins amounted to 121% for PGE2 and 125% for PGF2 alpha, within 3 hrs they decreased to control values. Decrease in activity of PGE2 and PGF2 alpha-synthetases was shown to depend on MEA concentration in vitro. Possible mechanisms of the radioprotector effect at various steps of the prostaglandins biosynthesis are discussed.

[Changes in prostaglandin systhetase activity in mouse tissues as affected by S-[N-(3-aminopropyl)-2-aminoethyl] thiophosphoric acid]. / Izmenenie aktivnosti prostaglandinsintetazy v tkaniakh myshei pod vliianiem S-[N-(3-aminopropil)-2-aminoétil] tiofosfornoi kisloty.

Effect of various concentrations of a radioprotector S-[N-(3 aminopropyl)-2-aminoethyl] thiophosphoric acid on the activity of prostaglandine synthetase was studied in mouse liver microsomes as well as in the soluble fractions of testicules and brain in vitro. The activity of prostaglandine synthetase was estimated by monitoring the formation of labelled PGF2 alpha and PGE2 from I-14C-arachidonic acid. The radioprotector at concentration 1.66 mg/ml stimulated formation of PGF2 alpha in all the tissues studied. At the lower concentrations of the radioprotector only slight stimulation of the biosynthesis of prostaglandines in testicules was noted. No effect on their synthesis in the brain soluble fraction could be observed while in the liver microsomes it was inhibited. The radioprotective substance studied apparently affected the cyclooxygenase activity, which is a key enzyme in the prostaglandine-synthesizing system.