Document vB38B3gxBRomDGoyrbrqk6Kam

0 GENETI C A EOLONICA Yol. 29 1888 No. 2 A i i THE .EFFECT QE ORALLY APPLIED AQUEOUS SOLUTIONS OP TEAT) AND zmc OH CHROMOSOME ABERRATIONS AND .INDUCTION OP SISTER CHROMATID EXCHANGES IN THE RAT {BATTU8 sp.) s ELZb IETA KO WALSKA-WOOHNA, LANINA MONIUSZICO-JAKONIUK, ELZBIETA KTJLIKOWSKA, KIRA MINIUK* Department ofBiology, Jilalysfcok BrancH of Warsaw TXahr.ersity* Department of Toxicology, Medical Acailemy, Blalystpk: "-A- n'-'t".V r - '. v - Tv. Summa ry. The influence oforally applied aqueous solutions of lead and zinc as well as its combinations on the occurrence of chromosome aberrations in the rat has been stu died. A cytogenetic analysis was performed on the bone marrow ceils multiplied as a re sult of the initial culture. A routine test of chromosome aberrations and SCE test were used. The .action of lead present in the solution on chromosomes was expressed by the induction of a strong chromatin erosionand by chromosome pulverization. The presence of zinc in aqueous solution first of all induced structural chromosome aberrations, par ticularly chromatidgaps. The.frequency offragments exchange befcweensister chromatids also significantly increased. The application of aqueous solution containing zinc after 6-week treatment of animals with solution with lead significantly reduced a genotoxic lead effect. Biological aspects of the obtained results are presented. T.end is a protoplastic poison, which, easily forms complexes with amine and carboxyl groups leading tp enzyme inactivation and disturbance of structural protein functions in the cell' (Dutkiewicz 1974). An effect of its action are dis turbances in different systems, snob as: central nervous system (Kitte.l 1983), alimentary tract system (Szewezrkowski 1957), kidneys and cardiovascular system (Kittel 1983) and erythrocyte system, where special affinity to bone marrow was displayed by lead (Gawlicka 1980), Workers of refinery, .electrotechnical, textile, gum industries, graphical plants, non-ferrous metalurgy, as well as drivers are occupationally exposed the most to a toxic action of lead. Zinc is a trace element necessary for normal development of plants, animals and people. It enters into the composition of polymerase of DNA and RNA as well I t \ 1 Received for publication: April 1987. The paper was presented at the Symposium IX of the Polish Genetics Society, Gdansk 19.88, September 1 - 3. 3 First author; Sr, Present address: ul. Swierkowa 20B, 15 - 950 Bialystok, Poland. Second author: Doc. Dr. hab., third and fourth authors: M.Se, Present address: ul. Mickiewicza 2c, 15-222 Bialystok, Poland. ^ 27046 1.82 E- Kowalska-Wochna efc al. C2] as thymidine Irinase (Byezkowska 1962). It has been found that zinc has a pro- tective action in relation to toxic effects induced by lead in erythrocytes (Ejnelli etal. 1975, Cerklewski 1976, Papaioannon etal. 1978, Abdulla 1980, Flana gan et al. 1982, -Cerklewski 1984, Chiba, Kikuehi 1984, Chiba, Kikuchi 1985). Lead inhibits a number of enzymes of heme biosynthesis, including de- hydratase of delta-aminolevulinic acid (ALA-D), whereas treatment with zinc caries restoration of that enzyme under in vivo and in vitro conditions. Ruither et al. (1977) displayed that a toxic effect of lead chlorate on macrophages in mice in vitro is smaller in the presence of zinc ions. s'' The present paper contains results of the studies on the effect of lead and zinc on the occurrence of chromosome pathology in the rat in vivo. MATERIAL AND METHODS The studies were carried out pn rat males and females of the race Wistar with the weight about 200 g, - The animals were randomly divided into 5 diagnostic groups, separately among males and among females. Dosage; Croup 1 -- Pb, 500 ppm for 6 weeks in the form, of lead acetate in drinking water, Group 2 -- Zn, 240 ppm for 14 days in the form of zano chlprate, Group 3 -- Pb+Zn, Pb 500 ppm for 6 weeks, then zinc 240 ppm for 14 days, Group 4 -- Pb+H20, Pb 5.00 ppm for .6 weeks, than water for 14 days. Group 5 -- water control -- the animals had only water throughout the -experiment. Each group consisted of 4 animals;-- 2 males and 2 females. Twenty four hours after the last dose, the animals were anaesthetized by ethyl eter and material was taken forstudies. A cytogenetic analysis was performed on the basis of cultured hone marrow cells. In each case, there Were 2 versions of culture -- routine and with the addition of 5-bromode.oxyuxicline of (BrdU) for the analysis of induction of sister chromatid exchanges (SCE). The cultures were conducted on the nutrient medium consisting of Eagle's fluid, bovine serum and antibiotics (all manufactured in Poland). It has been found that the optimal time of culture is .2.8 - 31 hours. It makes possible to obtain cellsafter2 replication cycles, which is important- for sister chromatid differentiation, as well as a sufficient accumulation of cells. Colcemid (Serva) was added 30 minutes before the planned end of culture, Golcemid in the amount of 0.2 ml was added at the concentration of 10 pg/ml to the culture having the volume of 10 ml. . Cytogenetic preparations were made according to the traditional method using 0.075 M EC1 as hypotonic fluid as well as Carney's solution (methanol and ice-cold acetic acid 3 :1) as a fixator. ; If f Ij ] 1 f | J f j f i | s i ? ? DUP040007575 fS] The effect of orally applied aqueous solutions of lead and zinc .1.83 Tlie culture with BrdTJ;was supplemented with 0.1 ml of that compound per 10 ml of the nutrient medium (0.2% was a working concentration of Brd IJ). The techni que of Perry and Wolff (1974) was employed to obtain differentiation in the sister chromatid dyeing. In the preparations from rbntine cultures SO random metaphase plates in the field of vision were analysed in each case. In the ease of SCE shiftings of chromosome fragments were counted in ail encountered metaphases with differentiated sister chromatids. The number of SCEawas counted per 1 metaphase plate and per 1 chro mosome for each studied group. A statistic analysis of the results was performed by the ^-Student's test (test for '' two means from small samples). RESULTS Group 1. (Pb .500 ppm). The most frequently encountered abnormality was the pattern of chromosome contour broadening with a simultaneous chromatin washing (that chromatin formed sheaths round the chromosomes and entire metaphases). The chromosomes showed weak stainability. In many cells that effect began from the middle of a metaphase plate causing uneven intensive chromosome staining within it (Pigs 1 and 2). The degree of erosion was different in individual metaphases,. In cases, where contour broadening was smaller, aberrations of the chromatid and chromosome type with the presence of acentric fragments was observed. Chromatic erosion occurred in 53.5% ofcells. Besides that, 35% ofcells displayed the state of. a still stronger destruction consisting in chromosome pulverization. In some metaphases that was a complete degradation, whereas in others it was par tial (Pig. 3 end 4); As compared to the control these results were statistically signi ficant, Chromosome aberrations were few and in relation to the control were statis tically insignificant. Group 2. (Zn 240 ppm). Tbe observed effects of zinc action are first of all structural aberrations of chromosomes (chromatid and chromosome gaps and breaks). A num ber of metaphases dipslayed simultaneously all tbe mentioned types of aberrations, and for that reason tbe number of these abnormalities was given per I metaphase plate. Tbe aberration level multiply exceeded not only the control values, but ..also those detected in the remaining studied groups. The mosjfc numerous were chromatid gaps. They were observed in .148 out of 200 analysed cells, which constitute 0.74 gaps per cell, while the control value was 0,5 gap/eel1. Statistic calculations in that case showed the largest significance level among all tbe observed changes in individual groups. Chromatid and chromosome breaks Were 0.42 .and 0-21 per cell, respectively, and were also statistically significant in relation to the control. Treatment with zinc in the amount of 240 ppm did not cause chromosome pul verization, and the frequency of chromatin erosion was similar to that of the control and statistically nonsignificant. DUP040007576 184 E. Kowalska-Woohrta et el. m Group B. (Pb 500 ppm, Zn 240 ppm). Lead intake for 6 weeka followed by zinc in takefor 2 weeks, cause erosion and chromosome pulverization in similarproportions -- 44% and 38% of cells, respective^. These values were statistically significant. It was found that in this group the degree ofthe chromosome contour broadening decreased, which markedly improved the quality of metaphase plates in comparison to group 1 (56 out of88 cells with erosion displayed a lower degree of injuries). The frequency of structural chromosome aberrations was statistically insigni ficant to the control. Table 1. GhromQaonaj.1 Aberrations in rat bene marrow cells after she treatment with Pb and Zn Treatment . . No. of animalB Pb .4 Zn 4 Pb+Zn 4 Pb+H.O HtO .4 4 Tfq. of cells analysed erosion no. % 2QQ 107 53.5 200 (35) 17.5 88 : 44.0 200 (56)* (28) 178 mo 200 (69) (34.5) 200 (38) (19.0) Changes observed pulverisation otoomatid gaps no. . % no. per ceil 70 35.0 6 0.03 - .148 0.74 chromatid, breaks no. per cell 6 0.03 .85. 0.42 chromosome bxeaks no,: | per cel! .. 4 0.02 42 0.21 76 38.0 5 0.025 5 ,0.025 i 0,005 17 8.5 1 0,005 - - 2 0.01 - 9 0.05 4 0.08 7 0.035 * The bracketed numbers ehorv a frequency of cells with a little erosion , ;j Table 2. Sister chromatid exchanges in the rat bone marrow cells after 1 the treatment with Pb and Zn Treatment ; :Ko. of animals Pb ' Zn Pb+2n Pb+fi.O H,0 j 4 4 4 4 -4 Total cell scored 34 58 85 40 100 Number of chromo somes SCE. ' 1428' .2436 3570 1680 4200 123 285 360 .147 .340 SCE per chromosome' per .cell 0.087 0.116 0.111 0.087 0.081 ;3.01 4.91 4.24 3.67 3.40 The number of chromosomes was obtained hr multiplying the total cell scored by 42, i.e. the number of chromosomes In diploid rat cells. Group 4. (Pb 500 ppm, H20). The percentage of cells with erosion in that group was extremely high and statistically significant (178 cells ont of 200 analysed ones). It, should, however, be emphasized that the percentage of chromatin destruction in many cells was clearly smaller than that observed in group .1 (in 69 put of 178 cells with erosion the" chromosomes preserved their shape with a slight chromatin washing making possible a cytogenetic analysis). Pulverization and fragmentation was re vealed only in 3.5% of the cells, but that result was statisticafiy significant. An analysis ofinduction ofthe sister chromatid exchanges in the studied material showed a statistically significant difference in ihel>GEs number/eell between ail the experimental groups and the control group. The largest significance was revealed WST DUP040007577 ,vith visible ***** <* chromosome contours i the control part Fig. !. A metaphase plats ' weeks) DUP040007578 i*-/ $ * % > % - I i ; ' "- ; ' .vs. .. ^ ill Fig. 3. A residue of a metaphase plate, in.-which the largest portion of chromosomes underwent pulverization (Pb 500 ppm, 6 weeks) . v,-Vf '%-SSf.'- m K- II ...Vr : VC.": . -- A" t* \ :M Jig. 4. A metaphase plate, completely pulverized {Pb 500 ppm, 6 weeks! .. DUP040007579 if ! / Pig. IS. A metaphase plate with sister chromatid differentiation (SOE test) in the case of lead and fcinc action (Pb 500 ppm, 6 weeks and Zn 240 ppm, 14 days) DUP040007580 J0 dof the ace- snic got. iase ter sest tTP ase, yed :onrms s is tal. eek the Mthe ctiisea lies ffcer fces. ski pm get illi tec an, out i of iac se- ere the pe rn, The effect of orally applied aqueous solutions of lead and g$no 185 in the groups -with zinc (groups 2 and 3). The numberqfSCBs/eell in these groups was 4.91 (Zffi) and 4.24 (Fb-f-Zn), while the control frequency was 3*40 SCEs/eell (Fig- 5) (Tables 1,2). Results obtalnedte male andfemale rats were similar. DISCUSSION An analysis ofresults ofthe studies on lead and zinc effect upon rat chromosomes'' has revealed .certain abnormalities. An undoubtedly characteristic effect oflead ac tion at the rate of 50,0 ppm for 6 weeks is washing of chromosome chromatin and in part of the cells -- a more advanced destruction in the form of chromosome pulve rization. The cytogenetic analysis in the present paper Was carried ont on the hone marrow cells. As it is well-known, lead displayes the largest affinity to marrow (Qawlieka 1980). The lead level in the marrow exceeds 50-fold the content ofthis metal in blood. H the lead concentration in blood is 7.0 - 130 pg/100 ml that in bone marrow attains 4200 - 9200 gg/100 g of tissue (Dutkiewicz 1974, Gawlicka 1980). Ibis undoub tedly affects the processes taking place in marrow, including also the state of genetic information and the rate and regularity of cell divisions. Reports of the literature are focused mainly on cytogenetic studies among people occupationally exposed to the action of increased lead doses (Schwanitz et al. 1970, Forni, Seeehi 1972, Schwanitz et al. 1975, Forni et aL 1976, Forni 1980, Forni et al, 1980). The material for these studies consisted ofperipheral blood, i.e. of uneompaEable tissue with regard to affinity to lead cumulation. The authors of these studies have revealed an evident increase in the frequency of structural aber rations of the chromatid type. Schwanitz et al. (1970) additionally observed spiralization. defects and chromosome pulverization. Other authors did not confirm the occurrence of chromosome aberrations with regard to lead in industrial exposition (Baucbinger et al, 1972, O'Riordan, Evans 1974). The present studies have shown that lead does not cause significantly increased frequencies of structural chromosome aberrations. An explanation of that may be the fact that the metaphases had strongly broadened contours and tjjs chromosomes were little stateable, due to which they were insufficiently "readable" for a cyto genetic analysis. As a matter of fact, more breaks were observed te the eases, where erosion was weak, which permitted to esfcimatethe ehepmosome structure. Therefore, the ability of lead to Induce chromatid and chromosome breaks in the bone marrow cells cannot be completely negated. Improvement of the metaphase plates quality after putting away lead and application of 1.4-day water break (Pb+H20) indicates that changes induced by lead do not inhibit cell ability to regeneration and may be reversed to a certain extent. A significant increase te the frequency of structural chromosome aberrations te blood lymphocytes under the effect of lead was revealed by Deknudt t al. (1977) S Genetics Polordca 2/88 DUP040007581 186 B. Kowalska--Woohna et al. 16] in a long-lasting experiment on monkeys in vivo, whereas a slightly increased Ievel.of chromosome fragments was detected: in human lymphocytes cultured, in .vitro in the presence of subtoxie doses of salts of different heavy metals including also lead ace tate (Deknudt, Demi.natti 1978), The first experimental work, which paid attention to a. possibility of mutagenic action oflead in vivo was a publication by Muro and G-oyer (1969). Mice orally got 1% of lead acetate in food. In the marrow cells there occurred a significant increase ofchromosome gaps and breaks."Ofinterest is the interpretation ofchromosome aber ration. induction by lead contained in the workofthe mentioned authors. They suggest that lead may act on repair mechanisms of cell by exerting a negative effect on ATP and protein synthesis or may activate a numberofenzym.es, particularly 3DNA-s.se, which causes damage to the genetic material. In our studies a special ability to induce chromosome aberrations was displayed by zinc. These were the only significant effects of that metal action. A similar con clusion follows from the work by Ei chhorn et al. (1973), who found that zinc forms stable combinations with various DMA groups, causing structural changes. This is important for normal functioning of nucleic acids. Zinc fed to absorb lead caused, a'marked weakening ofa toxic effect of that metal. The number ofregular metaphases increased, and most of the metaphaseshad a week erosion. This corresponds to reports from the literature. It is considered that the most sensitive index of lead poisoning i3 a decrease in dehydrogenase activity of del ta-aminolevulinic add (ALA-D) in erythrocytes (Chiba, Kikuchi 1985). In the experiments on rats it was shown that lead inhibits 80 - 90% of that enzyme acti ; i vity (Millar et al. 1970). An increase of zinc dose (above the required level) causes a marked reduction in lead absorption, which affects the lead level decrease in tissues and weakening of biochemical, effects (Cerkle wski, Ferbes 1976). Zinc feeding .after a 3-week treatment of rats with lead intensified lead discharge from erythrocytes. The speed of discharge increases proportionally to the zinc rate increase (Cerklewski 1984). The activity of ALA-D in Mood, strongly decreased by lead action (200 ppm for 2 weeks), comes back to the control level more rapidly in animals feeding larger zinc doses. Asimilar action ofzinc under in vitro conditions was displayed by Finelli et al. 19,75. The same conclusion was made by Chib a and Kikuchi (1984) for zinc and manganese action in vitro in. relation to toxic lead and tin effects in human, mouse and rabbit blood. Our studies show agreement with such suggestions and extend hypotheses about protective action of zinc with reference to a harmful action of lead On the state of genetic information. That may be related with the suggested participation of zinc in functioning of DMA and DMA. polymerases (Byczkowska 1962) and in conse quence with intensification ..of repair processes in cells. The analysis of SCE induction was very difficult, especially in group 1, where a large percentage of injuries by erosion metaphases Was noted. For that reason the number of analysed cells in that group is small. Troubles of a technical nature appe ared also in other experimental groups due to the occurrence of chromatin erosion, DUP040007582 . ff3 fzine uticaween foisoJeium lead. nntal Ltd., mieal 146. icino- r the )gC55- Post. . mulicity Hew 970). i and rung. ge in sis in ohro- .e toZen- ieher rO,, !XpO- Dora- EL the effect of.orally applied aqueous solutions of lead and sine 187 ft sister chromatids. ;. Differences in the SCB ntunber/cell as compared to the control were the largest in the case of action of zinc and zinc with lead. The presence of zinc, therefore, in creased SCE induction. In the remaining studied groups deviations from the control levels were smaller, but all of them were statistically significant. A negative re sult of the SCE test was obtained by Beek and Obe (1975) in human lymphocytes after the action of lead acetate 10-SM. ,' Unfortunately, the authors found the lack of mutagenic activity of lead salt, but stressed its highly harmful effect on developing fetus. Injuries may concern all the stages of organogenesis (Leonard et al. 1984). , Summing up the results in the present paper, it should be inferred that lead and zinc are metals with a high genotoxic activity in vivo, but interaction of zinc and lead weakens effects of lead action. Such a relation has not been found in the level of sister chromatid exchange induction. BEFBBEXCES 1. Abdulla M. (1980). Effect of oral zinc intake in lead poisoning. -Toxicol. Lett. (Amst.) Special Issue 1,25 (ahs.) 2. Bauchingor M,, Schmid ., Schmidt D. (1972), Chromosomen Analyse bei Verkehr-polizisten mit erho.ohter Bleilast. Mutation Boa. 16: 407 - 413. 3. Beek B,, Obe G. (1975). Thehuman leucocyte test system. VI. The use ofsister chromatid exchanges as possible indicators for mutagenic activities. Hurmngenetik 29: 127 - 134. 4. ByozkowskaZ. (1962),Trzypr2ypadkigoraozkicyakowej.MedycynaPracy 13: 207 - 213, 6. Cerklewski F. L., Forbes R. M. (1976). Influence of dietary, zinc on.lead toxicity in the rat. j. Nutr. 106: 689 - 696. 6. Cerklewski F, L. (1984). Fostabsorptive effect of increased dietary zinc On toxicity and removal of tissue lead in rats, J. Nutr. 114: .650 - 654. 7. Chi ba M., Kikuchi M. (1.984), The in vitro effects of zinc and manganese on delta-amino levulinic acid dehydratase activity inhibited by lead or tin. Toxicol. AppI, Pharmacol. 73: 388 - 394, 8. Chiba M., Kikuchi M, (1985). The in vivo and in vitro effects of manganese andzine On the activity of erythrocyte delta-aminolevulinic acid dehydratase. Nutrition Res., Suppl. 1: 568 - 571, 9. iPeknudt Qh., Colie A., Gerber G, B. (1977). Chromosomal abnormalities in lymphocytes from mbnkeys poisoned with lead. Mutation Bes. 45: 77 - S3, .10. Beknudt Gh., DeminattiM. (1978). Chromosome studies in human lymphocytes after in vitro exposure to metal salts. Toxicology 10: 67 - 75, 11. Dutkiewicz T. (1974), Cliemia toksvkologiczna, PZWL, Warszawa. 12. Eichhorn G, L., Berger .N, A., Butzow J. J. (1973), Some effects of metal ions on the structure and function of nucleic acids. Metal Ions in Biological Systems: .43 - 66, Plenum Press, New York. ! f t i DUP040007583 18$: E. Kowalska-Woelma et al. - Fihelli T.M., KJ.aiu.der D. S., KaraffaM. A., PeteringiEL fi, (107), Interactionofzinc and lead on delta-aminolevulinate dehydratase. Biochemical and Biophysical Commanieations 65, 1, 303 - 311. Academic Press, Inc. 14. Flana.ga.n P. R., .Chamberlain M. J., Yalberg L. S. (1982). The relationship between iron a.nd lead absorption in humans. Amer. J. Clin. Hutr. 36: 823 - 829. 15. Forni, A., Sec;chi G. C. (1972). Chromosome changes in preclinioal and clinical lead poiso ning and correlation with biochemical findings. Proceedings of the International Symposium "Environmental Health Aspects of Lead", Amsterdam: 473 - 485. 16. Form A., Oambiaghi Q-., Secehi G. C. (1976). Initial occupations, lexposure to lead. Arch. Environ. Health 31: 73 - 78. 17. Forni A. (1980). Chromosomal effects oflead. Acritical, review. Reviews on Environmental Health, Ed. G. V. James. Scientist; Publications Division Freund Publishing House Ltd.* Yol. HI, Ho. 2: 113 - 129. . 18. Forni A., Sctame A, BertazziP. A., Alessio L. (19.80). Chromosome and biochemical studies in women, occupationally exposed to lead. Arch. Environ. Health 35: 139 ? 146, 19. Forni A. (1984), Ghrotnosomal aberrations in monitoring exposure to mutagfcns-e'afcino* gens. Monitoring Human Exposure to Carcinogenic and Mutagenic Agents. IARC Scienti fic Publications Ho. 58. Eds. Berlin A., Draper M., HemminM K., Yainio SE. 20. Gawlioks B. (1980), Activity of nonspecific esterases in the marrow cells ofirats after the injection in mercury 'and lead. Fob Histochem. Cytochem. 4; 18, 277 - 285, 21. Kabata-Pendias A., Pendias H. (1979). Pierwiastki.sladowe w trodowisku hiologicznym. Wjdawnictwa Geologiczne, Warszawa. 22. Kittel M, (1983). Toksyhodynamika przewlekiych zatrad malymi dawkami olowiu. Post. Bag. Med. Dotw. 37: 325 - 356. 23. Erytoria zdrowotnatrodowiska. T.3. 016w. Praca zbiorowa. PWZL, Warszawa. 24. Leonard A., Gerber G. B., Jacquet P., Lauwerys R. R. (1984). Carcinogenicity, mu tagenicity,and tetrs,fcognnieiiy of industrially used metalls. Mutagenicity, Carcinogenicity and Teratogenicity of Industrial Pollutants. Ed. M. Eirsch-Volders, Plenum Press, Hew York, London. 25. Millar J. A., Battistini V., Cuming R. L, C., Carswell F., Goldberg A. (1970). Lead and delta-aminolevulinic acid dehydratase levels in mentally retarded children and in lead poisoned suckling rats. Lancet 2: 695 - 698. 26. Muro L. A., Gayer R. A. (1969). Chromosome damage in experimental lead poisoning. Arch. Path. 87; 660 - 663. 27. O'Riordan 3ff. L., Evans H. J. (1974). Absence of significant chromosome damage in males occupationally exposed to lead. Mature 247: 50 - 53- 28. Papaioannou K., Scihler A, Pfeiffer C. 0. (1978). Reduction of blood lead levels in battery workers by zinc and vitamin C. -J. Orthomol. Psychiatry 7:1 - 13. 29. Perry P., Wolff S. (1974). Hew Giemsa method for the differential staining of sister chro matids. Nature (Land.), 251: 1.56 - 158. 30. Ruither H.; Seemayr N., ManojlovioM. (1977), Einfluss von Ziak-Ionen anf die *oxisehe Yrirkung von Bleichlorid (PbCl,) untersucht an Mausemakrophagen in vitro, Zentralbl. Baktericfl. (Orig. B) Hyg. 164: 90 - 98. 31. Sohwanitz 6-., Lehnert G., Gehhart E, (1970). Chromosomenschaden bei beruflicher Bleibelastung, Dtsch. med. Wschr. 95: 1636 - 1041. 32., Schvranitz G., Gebhart E., Rott H. D., Sehaller K. H., Easing H. G., Hauer Q., Prestele H. (197S)i Chrcmosomenuntersnchungen bei Personen mit beruflicher Bleiexposition. Dtsch, med. Wschr. 100: 1007 - 1011. 33. Szewezykowski W. (1957), Symptomatologia wczesnej olowicy i wartosc badan labors, toryjnych w jej mzpoznawahiu. Anna!. UMCS. VII, 8: 173 - 217. DUP040007584 [9] The effect of orally applied aqueous solutions of lead .and sine .189 WPtYW PODAWAHEGO DOUSTHIE OLOWITJ I GY.NKV W ROZTWGRZE WQDIJYM h a P0W3TAWAHIE ABERRACJICHROMOSOMOWYCH ORAZINDUKCJE WYMIAITY CHROMATYD SIOSTRZAHYCH V SZCZTJRA {HATTUS so.) Streszczenie Badano wplyw podawanego dousfcnie olowiu, cynku oraz kombinaeji fcyeh metali w rpz- tworze wodnym na powstawanis abeiracji ehronsosomowych u szezura. Analizg eytogenetyczna przeprowadzono na komdrkaeh szpilcn kosfcnego nanmozonyeh w wyniku hodowli piarwotnej. Zaetosowano mtynowy test analizy aberraeji ehromosomowych oraz test SCE. ^ Dzialanie olowiu w roztworzo przejawialo si? wywolywaniem silnej erozji ohroxnatyny oraz pulweryzacji chromosomfiw. Obecnosd cynku wroztwnrze wywolywala przede wszystkiin abeira* i eje struktuxalne chromosomdw, szczegdlnie przerwy chromatydowe. Znamiemds zwipkszala si? j tez czstoc -wymiany' odcmkdw miijdzy chromatydami siostrzanymi. Podawaaie roztfroru ! zawierajaoego cynk po uprzednim podawaniu zwierz^tom roztwoni z olowiem wyraznie zmniej- Szalo genotoksyezny efekfc olowiu, Przedatawiono aspekfcy biologiczne uzyskanych wynikdspj; . ~ a :* - ; ' . {> i JSJWmm HEPOPAJ1BHO IIOAABAEMKDC BOj(HHX PACTBOPOB CBHHIJA H IIHHKA HA 0BPA3OBAHKE XPQMOeGMHMX ASEPPAHHit H HHffyKHJffO CECTPHHCKOrO XPOMATHffHOrO OBMEHA Y KPBIC {BATTT3S sp.) Pe3WMe HccaeftoBaiioci bo h s h h c nepopantHo noflafiaewwx eo h h ebc pactEOpoB CBumia, BEHza, a "raiws .KOMduHanua CBHHtta c u h h r o m sa ofipasoBaiiae xpOMocoMBBtx a6eppanHk y Kptic. IRcroreneraaecKHS aaajiHa npoBojcraca na Knencax KpcTHoro Moara, paBMnoaceHHMx b peayni/raTe nepawHoro pa3BegeHHjr. IIpaMeHeH pytHHHHfi: TecT aHaarna xpoMOCOMBiix adeppapak, a xaEKe Teer SCE (cecTpzKCKHk xpoMa- raaM& o Gmc h ), Heacrsze CBHEtua, naxonirtnsrpca b b o h h o m pacxBope, npotfajumocb b cHUtfioSapoBHA xpoMaxHaa h b 0ym,BepH3aHHH xpoMpcoM. XIh e k , HaxopamHfica b pacTBope, BBiSbiBannpttKne Bcero ctpyKxypani.Htie aSepapHH xpoMocoM, oc.a6err.HO xpoMaTHHHsxe paspUBti, a TaKBce 3Ha<mTeni,Ho nOBtaman aacroTy eSwceHa 4>pameirroB Me*ay cecrpuHCKHMii xpoMaxHkaMH. IIoHaaa BOHHoro pacraopa nHHxa noons npegaapaTeatHoro 6-Henn>Horo nepopansHoro BBeneaaa k u b o t h b im CBHHna, Tax3ce b b o a h o m paciBope, eymecrb b h h o yMsnhmma. reHOTOKCHnecKHk 3#$sicr CBHHta.a, ITpenoTaBjieHH 6HOJjoriecxHe acnesTtt nonyseHHBK ,pe3yin>TaTOa. E DUP040007585