[Mechanisms of anti-cancer effects of plant polyphenols. II. Suppression on tumor growth].

Mechanisms of suppression of carcinogenesis promotion/progression by plant polyphenols have been considered. They can decrease cyclins and cycline dependent kinases and activate inhibitor proteins in tumor cells that results in cell cycle arrest. Plant polyphenols can induce apoptosis by modulating anti/proapoptotic proteins and also can inhibit tumor metastasis and angiogenesis. Polyphenols act through the regulation of cell signal transduction and gene expression.

[Mechanisms of plant polyphenols anti-cancer effects. I. Blockade of carcinogenesis initiation].

Mechanisms of anti-cancer effects of polyphenols, found in fruits, vegetables, spices and representing parts of daily nutrition, have been considered. These compounds may be the basis for development of cancer preventive preparations. They can block carcinogenesis initiation by inactivation of exogenous or endogenous genotoxic molecules including reactive oxygen species. Another mechanism consists in inhibition of activity and synthesis of carcinogen-metabolizing enzymes. Plant polyphenols also induce expression of antioxidant and detoxification enzymes genes.

[Magnesium homeostasis: mechanisms and inherited disorders].

Magnesium is one of the major cations of biological systems. It plays an essential role in many cell processes. The importance of magnesium underlines its maintenance under the steady conditions according to the metabolic state of the cell. In the present review mechanisms of magnesium homeostasis, that have been intensively investigated during last decades using both pathophysiological and molecular genetic approaches, are considered. Disorders of magnesium homeostasis resulted in development of magnesium-deficient conditions, which are commonly found in various diseases (diabetes mellitus, cardiovascular diseases, chronic fatigue, alcoholism, psychiatric and neurologic diseases, etc.), stress condition and therapy with some kind of drugs. Special attention is paid to familial hypomagnesemias caused by genetic defects of magnesium transport systems. Overview of clinical and biochemical characteristics of twelve familial disorders is given and mechanisms of inherited magnesium homeostasis disorders as well as nine identified and mapped genes responsible for their development are considered. These genes encode subunits of ionic channels, co-transporters, modulators of transport systems and receptors controlling either intestinal absorption or renal reabsorption of magnesium. Recent advances in mechanisms of magnesium homeostasis will lead to insights in diagnostics, preventive medicine and treatment of magnesium-deficient conditions.

[DNA protective activity of natural and synthetic antioxidants]. / DNK-protektornaia aktivnost' prirodnykh i sinteticheskikh antioksidantov.

Free radicals attack cell genome in oxidative stress conditions accompanying many human diseases. Mutagenic and carcinogenic xenobiotics cause oxidative DNA damages also. Oxidative DNA damages become intensive in aging organisms. The data on natural and synthetic antioxidants protecting DNA from oxidation are presented in this review.

[Benzimidazole derivative inhibition of the mutagenic activity of 2-aminoanthracene]. / Podavlenie mutagennoi aktivnosti 2-aminoantratsena proizvodnym benzimidazola.

The antimutagenic activity of a new benzimidazole derivative that has antioxidative properties was found in the Salmonella/microsome test. This compound reduced the level histidine revertants induced by the promutagen and carcinogen 2-aminoanthracene. Inhibition of the mutagenicity of 2-aminoanthracene appears to be associated with the inactivation of its genotoxic metabolites. The capacity of the benzimidazole derivative for antimutagenic effects is possibly due to a dihydroxyphenyl radical that is present in its structure.

[Free radical oxidation of DNA and its biomarker oxidized guanosine(8-oxodG)]. / Svobodno-radikal'noe okislenie DNK i ego biomarker okislennyi guanozin (8-oxodG).

Endogenous free radicals, in particular, reactive species of oxygen, nitrogen, chlorine cause DNA oxidation which is potentiated by exogenous prooxidant factors. The free radicals cause various DNA damages. This review highlights one of them, oxidative modification of guanosine, and also modern methods of the estimation of oxidized guanosine (8-oxodG) content. The numerous data on an induction of 8-oxodG in DNA by exogenous genotoxicants in vitro and in vivo are presented. 8-oxodG is used as a biomarker of DNA oxidation, accompanying some human diseases.

[Expression of the phospholipase C gene of Pseudomonas aeruginosa in Escherichia coli and Pseudomonas]. / Ekspressiia gena fosfolipazy s Pseudomonas aeruginosa v kletkakh kishechnoi palochki i psevdomonad.

The plc gene for phospholipase of Pseudomonas aeruginosa, able to be transcribed only from its own promoter, has been introduced into Escherichia coli, Pseudomonas aeruginosa and Pseudomonas putida cells in the recombinant plasmid pPMS21 of a wide host range. The expression of plc gene in all recipient cells has been shown to be phosphate regulated. The fact emphasizes the identity of pho-regulation systems in Escherichia coli and Pseudomonas cells. The level of phospholipase activity is similar in Pseudomonas putida and Pseudomonas aeruginosa under the conditions of the gene derepression, while in Escherichia coli cells the level does not exceed 10% of activity registered in Pseudomonas cells.