[Effect of saccharol glycosides on energy metabolism in animals with abnormal carbohydrate tolerance]. / Vliianie glikozidov sakharola na énergeticheskii obmen u zhivotnykh s narushennoi tolerantnostíu k uglevodam.

A trial has been performed of a new sweetening agent saccharol, glycosides complex, on energy metabolism in rats with experimental alloxan diabetes. Elevated glucose level observed in rats with insulin insufficiency was associated with hexokinase activity inhibition and changes in the activity of the enzymes involved in glucose-6-phosphate transformation: enhanced activity of glucose-6-phosphatase and glucose-6-phosphate dehydrogenase against inhibition of phosphoglucomutase activity. Introduction of saccharose aggravated the above shifts in the rat liver, whereas saccharol possesses a protective action on hexokinase hepatic reaction and enzymes of glucose-6-phosphate conversion, reduced blood glucose. Positive changes induced by saccharol on energy metabolism in animals with insulin insufficiency can be attributed to the effect of saccharol glycosides.

[Effect of a new sweetening agent from Stevia rebaudiana on animals]. / Vliianie novogo podslastitelia iz dvulistnika sladkogo na organizm zhivotnykh.

Animals received saccharol adequate (by sweetness) to sugar, and in 10- and 50-fold increased amounts. The data of chronic 10-month experiments studied in the time course after 2, 5, 10 months have permitted a conclusion that saccharol included into the ration during long periods, does not produce a significant effect on the parameters of metabolic processes and morphological picture of the internal organs in test animals. Saccharol in 50-fold increased amounts inhibits the activity of oxidative phosphorylation in the hepatic tissue of rats.

[Inhibiting effect of the polyphenolic complex from Plantago major (plantastine) on the carcinogenic effect of endogenously synthesized nitrosodimethylamine]. / Ingibiruiushchee vliianie polifenol'nogo kompleksa iz podorozhnika bol'shogo--plantastina--na kantserogennyi éffekt éndogenno sintezirovannogo nitrozodimetilamina.

Amidopyrine administered in combination with sodium nitrite in the long-term experiment produces the toxic damage of the liver and tumors in rats in connection with endogenic synthesis of carcinogenic nitrosodimethylamine. The inclusion into the animal diet of the polyphenolic complex from Plantago major--plantastine as an inhibitor of the carcinogen synthesis reduced the toxic damage of the liver that was indicated by normalization of biochemical parameters and also decreased the tumor yield from 87.5% to 33.3%. The data obtained may be the basis for the combined use of plantastine with nitrosated drugs that would contribute to carcinogenesis prevention.

[Food inhibitors of the formation of carcinogenic nitroso compounds]. / Pishchevye ingibitory obrazovaniia kantserogennykh nitrozosoedinenii.

A study was made of the effect of plant preparations, pectin, plantastin, tiliaflan, cholosas and carbonic acid phytoextract from the fruit of the Umbelliferae family (CO2-EP) on the synthesis of carcinogenous nitrosodimethylamine from amidopyrine and sodium nitrite. Gas chromatography made in vitro and in short-term experiments on animals demonstrated plantastin to display an inhibitory action, which was less marked for tiliaflan, CO2-EP and cholosas. The system of experiments in question may be recommended for preliminary screening of the inhibitors of nitrosation with a purpose of using them for the prophylaxis of carcinogenesis induced by nitroso compounds.

[Possibility of endogenous dimethylnitrosamine synthesis in rats administered dimethylamine and nitrite with the food]. / Izuchenie vozmozhnosti éndogennogo sinteza dimetilnitrozamina pri vvedenii krysam s pishchei dimetilamina i nitrita.

Concurrent peroral administration of dimethylamine (DMA) and sodium nitrite to rats produced necrosis of liver parenchyma and increased the activity of glutamicoalanine transaminase. Similar changes were recorded after administering dimethylnitrosamine (DMNA) that points to potential synthesis of this carcinogen from the precursors. Prolonged (over 2.5 years) feeding with DMA and nitrite resulted in part of the rats in tumours of the lungs and in other neoplasms. Ascorbic acid that blocks the endogenous synthesis of DMNA interfered with the development of tumour and pretumour lesions that emerged as a result of concurrent feeding with DMA and nitrite.

[Influence of precursors of endogenously synthesized dimethylnitrosamine on the activity of the demethylase of that carcinogen in rat liver]. / O vliianii predshestvennikov éndogenno sinteziruemogo dimetilnitrozamina na aktivnost' demetilazy étogo kantserogena v pecheni krys.

Oral administration of dimethylamine, sodium nitrite and a combination of these precursors of endogenously synthesized dimethylnitrosamine to rats increased the activity of demethylase of this carcinogen in the liver microsomes. Under conditions of chronic experiment inclusion of dimethylamine into the diet of rats intensified the demethylase activity even in the presence of casein, an inductor of this enzymatic system. An inhibitor of protein synthesis--actinomycin D prevented an increase of demethylase activity in the microsomal fraction caused by dimethylamine.

[The effect of a long-term administration of fluorine with food on the carcinogenesis and biochemical changes in the liver of rats]. / Vliianie prodolzhitel'nogo vvedeniia ftora s pishchei na kantserogenez i biokhimicheskie izmeneniia v pecheni krys

The effect of different amounts of fluorine in the ingested food (1.5 and 5 mg per 1 kg of body weight) on the development of tumours and biochemical changes in the liver of rats with carcinogenesis caused by their feeding on DAB was studied. With a long-term administration of fluorine in a dose of 1.5 mg/kg the appearance of macroscopically visible tumours in the liver proved less notable than with a lower dose or complete absence of fluorine. With carcinogenesis the rate of glycolysis in the liver of rats increases. A relationship between the inhibiting action of sodium fluoride on the glycolysis and changed activity of phosphofructokinase has been ascertained.