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Environmental and Molecular Mutagenesis - Legacy Tobacco ...

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64 1989 EMS Abstracts<br />

http://legacy.library.ucsf.edu/tid/clb93d00/pdf<br />

Note s 24 hour after treatment using 5 animals per group . The test compounds did not<br />

increase the frequencies of MNFCEs . The preliminary in vivo CA-tests were<br />

carried out at 6, 24, 48hours after administration . The frequencies of polyploid<br />

were 0-3 .5% <strong>and</strong> were not different from control . Furthermore, the effect of<br />

thes chemicals on polymerization of tubulin was examined . These compounds did<br />

not inhibit specifically tubulin polymerization to microtubules . Therefore, in<br />

vitro induced polyploid can not be mediated through the microtubular system .<br />

(1)Ishidate,M . et a1(1988) Mutation Rea . 195 151-213 .<br />

180<br />

MUTAGENIC ACTIVITY, DNA BREAKAGE AND SOMATIC MUTATION OF ARENEQUINONES .<br />

H . Furukawa, K . Kavai, T . Miyazawa <strong>and</strong> T . Sato, Meijo University, Nagoya(Japan), Tohoku<br />

University, Sendai(Japan), <strong>and</strong> Inaba Biophoton Project, Research Development<br />

Corporation of Japan, Sendai(Japan) .<br />

it was reported that arenequinone was synthesized photochemically by sunlight<br />

irradiation from corresponding arenas . The mutagenic activity of 3,6-banzola)pyrenequlnone,<br />

1,6-benzota]pyrenequinone, 1,6-pyranequinone <strong>and</strong> 1,8-pyrenequinone are 44, 77,<br />

91 <strong>and</strong> 298 revertants on Salmonella typhimwrdun TA100 without S-9mix . . It was<br />

considered there must be the other mechanism with the exception of epoxide formation .<br />

Futhermore breakage of DNA such as pBR322 or A phage DNA by 1,6-pyrenequinone or 1,8pyrenequinone<br />

were suppressed by active oxygen scavenger such as buthylhydroxytoluene,<br />

glutathione, a-tocopherol, sorbitol <strong>and</strong> L-aacorbic acid in vitro . Therefore we<br />

considered that both mutagenic activity <strong>and</strong> DNA breakage activity were caused by active<br />

oxygen molecules <strong>and</strong> the like . Small single spot frequency in Drosophila wing spot test<br />

by 1,6-pyrenequinone, 1,8-pyrenequinone, 1,6-bento(a]pyrenequinone <strong>and</strong> 3,6-benzo(aJpyrenequinone<br />

were risen about two fold of control's frequency . Then it was considered<br />

active oxygen molecules caused the somatic mutation of Droeoph{la melanOgaster . For the<br />

reason above mentioned phenomena, we considered that the planar ring surface of arenequinone<br />

molecules are x-electron deficient, <strong>and</strong> toxic arenequinones contain<br />

considerable radical structures in the resonance formulae . And we would like to<br />

emphasize the urbane airborn particulate containes a few arenequinones <strong>and</strong> toxic<br />

arenequinones should be formed by sunlight irradiation from corresponding arenes .<br />

TRANSPOSITION : EFFRCTg AND MECtlAMISMS<br />

David J . Galas <strong>Molecular</strong> Biology, University of Southern California, Los Angeles, CA<br />

90089<br />

Transposition of mobile genetic elements is apparently a universal phenomenon<br />

occurring in the genomes of all organisms . Certainly in all the experimental organisms<br />

common to the genetics laboratory, they have been extensively characterized . The list<br />

begins with maize, of course (McClintock, 1956), <strong>and</strong> includes Drosophila, 8aecharomyces<br />

Caenorhabditis <strong>and</strong> several different types of bacteria . The genetic effects of mobile<br />

elements are diverse <strong>and</strong> include the induction of insertion mutations, deletions,<br />

inversions <strong>and</strong> other rearrangements, <strong>and</strong> the turning off <strong>and</strong> on of gene expression . In<br />

this talk, I will discuss several examples of the ways in which the mobile elements can<br />

cause these effects . I will draw examples from observations <strong>and</strong> experiments in several<br />

systems, but will focus on bacterial systems in discussing specific mechanisms . The<br />

bacterial insertion sequence, IS1, has been studied to determine the molecular<br />

mechanisms of the transposition process, the component parts of the molecular<br />

apparatus, <strong>and</strong> to dissect the specificity determinants of the protein <strong>and</strong> DNA<br />

components .<br />

GFW=CITY OF VANADIUM CCt1QC[[RNID6<br />

A . GaLLI, L . GIHCKDR, R . DEL CARFA2WE, C . DELIA CPDCE <strong>and</strong> G . BI+DNZETTI<br />

Instituto di Mutagenesi e DifferenziamenYa CIIIR PISA ITALY<br />

181<br />

182<br />

Acmnnium Metavanadate <strong>and</strong> Vanadyl Sulfate were tested for their ability to induce mitotic<br />

gene oonversion <strong>and</strong> point reverse uutatian in the D7 strain of S . oerevisiae . Metavanadate<br />

increased the convertant <strong>and</strong> revertant frequencies <strong>and</strong> the highest ac v ty was observed<br />

without metabolic activation . This indioates that S9 hepatic fraction <strong>and</strong> cells fron logphase<br />

oantainirg a high level of cytochreme P-450 biotransform vanadate probably reducing<br />

it to vanadyl . Vanadyl did not induce any genetic effects in the same experimental conditions<br />

An increase of gene conversion <strong>and</strong> point mitation was induced by vanadyl in cells<br />

fraa log-phase, suggesting that these cells are able to axidate vanadyl to vanadate . To<br />

explain our results, we hypothized that matavanadate is the genetoxically active form <strong>and</strong><br />

the monooxygenase system is involved in biotransfotmntion of varadiun, particularly reduoing<br />

vanadate or oxidatiry vanadyl . To confirm this hypothesis, years cells harvested fram<br />

lod-phase with high level of cytochrane P-450 were treated with metavanadate <strong>and</strong> vanadyl<br />

50869 3576

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