[The effect of treatment of chrysotile with chloride iron (III) on the effect of genomic instability in cultured human lymphocytes].

All forms of asbestos are carcinogenic to humans, that caused the prohibition of its use in Europe, America, etc. However, the unique physical and chemical properties of asbestos and many opportunities for its applications in various industries and human activities require the creation of new technologies to. Analysis of genomic instability in human lymphocytes in a large range of doses (micronucleus test with cytochalasin B showed a decline of core indicators of genome instability (frequency of dividing cells with cytogenetic damage, asymmetry in the distribution of the genetic material in mitosis, proliferative activity) incubation of cells with asbestos modified chloride iron, as compared to the initial sample. These data are consistent with the results of analysis of the intensity of neutrophil chemiluminescence of luminol by exposure of human blood samples studied. Based on the findings made some practical recommendations to the protocol cytogenetic analysis of genomic instability of people exposed to asbestos.

[Chrysotile-asbestos induces cytogenetic effects in the rat's mesothelium in vitro and in vivo].

Under cultivation of rat peritoneal mesothelial cells in vitro in them there are appeared signs of the genomic instability, evidencing their transformation: increasing of the number of both binucleated cells with micronuclei and polynuclear cells and the increase of sizes and polymorphism. Asbestos greatly accelerates this process. Asbestos-induced carcinogenesis in vivo is accompanied in pleural mesothelium in the rats there also revealed with similar signs of genomic instability and cellular transformation.

[Carcinogenic and mutagenic activity of chrysotile, processed with iron chloride (III)].

This work is devoted to the study of the role of iron ions in the carcinogenic and mutagenic activity of chrysotile. For this aim natural chrysotile was treated with ferric chloride (III), washed, crushed and intratracheally introduced into Wistar rats. When administered to rats intact chrysotile induced mesotheliomas in 27,9 + 4,6% of cases, and chrysotile modified with ferric chloride - in 1,3 +/- 1,3%. Mutagenicity of the same samples was studied in the micronucleus test when administered intraperitoneally to mice Fl (CBA x S57Bl6). Polychromatic erythrocytes in the bone marrow were investigated 24 hours after intraperitoneal administration. The frequency of polychromatic erythrocytes with micronuclei was decreased from 7,4 +/- 0,18 by 1000 due to the action of chrysotile, from 2,8 +/- 0,42 for 1000 after the introduction of a modified sample. It is hypothesized that the ferric chloride modifies the surface of asbestos fibers that reduces the induction of free radicals which are the primary cause of and carcinogenic effects of chrysotile.

[Carcinogenic activity of the pesticide propoxur].

Wistar rats were fed propoxur in their diet at 0, 500, 3000, and 8000 ppm during throughout their life. The number of tumors was equal in the control and experimental groups. These were hemoblastoses and breast and uterine tumors. All tumors occurred spontaneously in the rats. A few experimental animals were found to have bladder epithelial hyperplasia that might be pretumorous; however, no bladder tumors were detected. It is concluded that the investigations revealed no carcinogenic activity of propoxur.

[Effect of peptone blocking asbestos-induced carcinogenesis in rats].

Regular intraperitoneal administration of peptone to rats was initiated immediately and 12 months after intraperitoneal thrice injection of crokidolite UICC in a dose of 20 mg. The rate of peritoneal mesotheliomas was 37.8% after co-administration of peptone and crokidolite, 25.6% following 12 months of crokidolite injection, and 72.1% after use of crokidolite alone. The effect of peptone administration is accounted for by the action of macrophages on transformed mesothelial cells and mesothelioma cells.

[Evaluation of the carcinogenic activity of phenol-free coal-tar creolin].

When orally administered to rats and mice, phenol-free coal-tar creolin containing 0.018+/-0.002 g/kg of benz(a)pyrene showed no carcinogenic activity. The discrepancy of the biological activity and content of carcinogen in the combined mixture, the role of their components in carcinogenesis, the value of control experiments, and historic control test, and the implication of these rapid tests in the evaluation of their carcinogenicity is shown.

[On decreasing carcinogenic activity of calcified chrysotile fibers].

When chrysotile fibers treated with Portland cement, Mg was partially substituted by Ca, therefore monolayer of Ca(OH)2 was formed as a cover, and that changed acidity force, number of active centers and biological activity (absent mutageneity, generation of active oxygen forms by macrophages was characterized by lower maximum and longer time to background level vs. native chrysotile).

[Impact of modification of the fiber surface of chrysotile on its biological activity].

Samples of commercial chrysotile-asbestos and asbestos cement, which were equal in number, were prepared. The content of fibers, up to 80 microm in length, was 87.4 and 85.0% in the first and second samples, respectively. Chemical analysis confirmed that there were cement components onto the surface of fibrils in the second sample. Onto the surface of native asbestos fibers, there were considerable distribution bands of active centers in the range of pH values of 5, 6.4, and 7.3; their largest number was at pH 6.4. Asbestos cement fibers had a band at pH 7.3, i.e. there was displacement towards the neutral region. Thus, their capacity for oxidative processes is likely to be lower than that in the fibers from the first sample. The mutagenic activity of the commercial chrysotile, examined in the micronucleus test, was substantially higher (p < 0.01) than that in the asbestos cement sample wherein it did not differ from that seen in the control experiment (saline solution). Mutagenicity was not found in cement and asbestos cement dust (2-3% of fibers) either. It is probable that the absence of mutagenicity in the cement-coated asbestos fibers may be attributable to a considerable reduction in their potencies for the formation of active radicals (oxygen, lipid peroxidation, and others).

[Characterization of the biological properties of acid-treated chrysotile-asbestos fibers].

Boiling of chrysotile of the textile brand PRZh1-50 in concentrated hydrochloric acid for 10, 15, and 20 minutes gave rise to three chrysotile-asbestos samples. The content of MgO decreased from to 24, 19, and 9%, respectively. As compared with the baseline values, the number and force of positively charged electrical centers were less in the samples containing 24 and 19% MgO and more in the sample having 9% MgO; the negatively charged centers were present in the former two samples and absent in the third one. When the samples were intrapleurally administered to rats, their hemolytic activity, induction of active oxygen radicals, mutagenic activity (micronuclear test using murine bone marrow cells), and the frequency of mesotheliomas were less in the treated samples than in the baseline ones; but there were no differences between the treated samples. Thus, the altered physicochemical properties of the fibrillar surface of asbestos diminished its biological aggressiveness; however, increased treatment rates failed to lead to its further decrease. There was no relationship of the biological properties to the number and force of electric charges of the surface.