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Environmental and Molecular Mutagenesis - Legacy Tobacco ...

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198 1989 EMS Abstracts<br />

_,_-- - .-<br />

Notes "`i`A"'the case bgtw&WINDEA <strong>and</strong> NDMA . With regard to detectability of minimum<br />

dose foEr a chemical using Tradescantia stamen hair system, this depends<br />

upon the kigl'6of chemical <strong>and</strong> test clones . It may be stated that<br />

an effective-8ase`for inducing mutations is in the order of picograms of<br />

chemicals per flower . Therefore, Tradescantia may be possible to use as<br />

one of the indicators for risk evaluation of chemical mutagens .<br />

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

MUTAGENIC EFFECTS OF ENVIRONMENTAL RADON<br />

Tavera L ., BalcBzar M ., de la Rosa M . E ., 2immering S .*<br />

ININ . Sierra MoJada N447 . 2 y 3er . pisos . Col . Lomas Barrilaco C .P .11010 .MEXICO<br />

*Brown University, Providence U .S .A .<br />

574<br />

The internal radon progeny exposure exhibits a distinct maximum dose In the respiratory<br />

tract Inducing lung cancer .<br />

From epidemiological data available only a statistical significance Increase of cancer<br />

frequency with Increasing background radiation can be deduced . Because of these data<br />

are given for different ages <strong>and</strong> radiation environments a Radon Chamber was desloned to<br />

exposure bioassays for searching effects other than cancer induced by radon exposure .<br />

The radon atmosphere in the chamber reach 97% of saturation after 19 days, however it<br />

is possible to determine an equivalent average radon concentration by means of Solid<br />

State Track Detectors . The Radon daughters assessment Is also possible with these detectors<br />

.<br />

Samples of Drosophila exposured in this Radon Chamber have shown inter-<strong>and</strong>-Intraspecie<br />

differences in sensibility when fecundity <strong>and</strong> viability were measured . Additionally a<br />

very typical aberrant phenotype was induced in D . melanogaster wild-type .<br />

575<br />

GENOTOXICITY ASSESSMENT OF QUINAPRIL, A NEW ANTIHYPERTENSIVE DRUG . J .C . Theiss, N .L .<br />

Kropko, G . Krishna, <strong>and</strong> V . Ciaravino, Parke-Davis pharm . Res . Div ., Warner-Lambert Co .,<br />

Ann Arbor, MI(USA)<br />

Quinapril was assessed for genotoxicity in a variety of test systems . This drug was<br />

not mutagenic toward S . typhimurium (10,000 ug/plate highest dose tested) <strong>and</strong> did not<br />

increase the mutant or SCE frequency in V79 cells (1400 ug/ml highest concentration<br />

tested) . Quinapril did not induce micronuclei in mice (1430 mg/kg high dose-80% mouse<br />

LD50) nor did it induce structural chromosomal aberrations (SCAs) in rats (2130 mg/kg<br />

high dose-rat LD10) . Thus, quinapril was not clastogenic in vivo at doses far in excess<br />

of the maximum human dose of 1 mg/kg . There was a slight but statistically significant<br />

dose-related increase in SCAs in V79 cells treated with quinapril for 3 hours which<br />

occurred in the presence of S9 only <strong>and</strong> at 18 hours post-exposure only (12, 18, 24, <strong>and</strong><br />

40 hour time points) . The maximun frequency of cells with SCAs detected (6t) was within<br />

the historical control range for this laboratory (0-6 .31 cells with SCAs, n-31) <strong>and</strong> the<br />

minimum concentration at which an increase in SCAs occurred (1400 ug/ml) was cytotoxic<br />

(

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