Environmental and Molecular Mutagenesis - Legacy Tobacco ...

194 1989 EMS Abstracts 69
Notes
II+cLUEhCE OF iiALIDI%IC ACID ON THE KILLING AND h1GTATION IiJDliCED BY UV
LIGiIT AP+D M~tiNG IN DENSITY INHIBITED V79 CELLb
Rita Gaosh(Datta), S. at a ^ and G . Bnaumik, 8aha Institute
of Nuclear ?nyeics, I ~, alt ake, Calcutta-700 064 .
Density inhibited plateau phase V79 cells after treatment with UV
light or N-metnyl-N'-nitro-N-nitrosoguanidine(13NNG) exhibited improvement
in survival accompanied by lowering of mutant yield (resistance
to 6-tnioguanine) on delay in trypsinization (20h) . If nalidixic acid,
an inhibitor of topoisomerase activity was present during tae period of
delay, survival levels were similar to tnose obtained on immediate
trypainization For mutational analysis, UV fluence was va 1ed from
4J/m` to 20J/m! ; corresponding mutant frequencies (per 10~ viable
cells) were 3 .0+0 .5 and 16 .9+0 .8 at these two fluences on immediate
trypsinization . On delayed trypsinization, tnesp values decreased to
1 .8+0 .6 and 13 .0+0 .5 respectively and again increased to 5 .5+0 .8 and
21 .a+0 .8 when nalidixic acid was present . In case of JSYtteG, tpe doses
varied from 0 .5µg/ml to 2 .Oµg/ml f3r lh treatment time ; the ccrresoonding
mutant frequencies (per 10 viable cells) were 7 .5+0 .5 and
32 .5t2•5 at these doses on immediate trypsinization . If tnB trypsinization
was delayed, the corresponding values were 4 .5±1 .0 and 23 .3+2 .2
respectively . However, wnen nalidixic acid was present during thle
delay period, tue values were 8 .5+1 .2 and 38 .8+2 .0 . The results indicate
the involvement of topoieomerase in repair of potentially lethal
damage .
195
IN SITU EVALUATION OF POTENTIAL GENETIC HAZARDS FROM CHEMICAL WASTE SITES .
B .S . Gill, J . Rice and S .S . Sandhu . EHRT, Research Triangle Park, NC 27709 and EPA,
Research Triangle Park, NC 27709 .
In situ monitoring of biological effects from chemical waste sites provides hazard
assessment under the complexities of natural environmental conditions . For such studies,
plant assays are cost effective and are ideal for preliminary investigations .
The studies reported here were initiated at The Fairway Six pesticide site in Aberdeen,
North Carolina and Palmetto Wood Preserving site in Dixiana . South Carolina using Tradescantia
micronucleus and maize vaxy locus assays . The chemical analyses of soil
samples from these sites indicate concentration of lindane (17385 ug/kg), beta BHC
(12645 ug/kg), and heptachlor (378 ug/kg) at four feet dbpths at the Aberdeen site and
arsenic (1292 mg/kg), chromium (1444 mg/kg), and copper (924 mg/kg) on the surface at
the Dixiana site . Results of Tradescantia micronucleus assays shoved significantly
higher frequencies of micronuclei from the contaminated plots as compared to the control
plots . Toxic effects for maize growth were observed on contaminated plots at
Dixiana site . The soil samples collected from these sites were analyzed in the laboratory
for their biological effects using Vicia root tip, wheat aneuploidy, and
Tradescatia micronucleus assays . Preliminary evidence confirms the in situ findings .
The sites have now been cleaned . The in situ and laboratory experiments vill be
repeated to evaluate the efficacy of the remedial operations . This is an abstract of
a proposed presentation and does not necessarily reflect EPA policy .
196
OXIDATIVE STRESS-INDUCED GENETIC INSTABILITY IN CULTURED CHINESE HAMSTER CELLS
J .J .P . Gille, C .G .M . van Berkel, F .A .J .M van de Klundert, and H . JoenSe . Institute of
Human Genetics, Free University, P .O . Box 7161, 1007 MC Amsterdam, The Netherlands .
Two different inducera of oxidative stress, i .e ., normobaric hyperoxia and H202
were compared with respect to their ability to induce strand breaks and gene muta-
tions .
Normobaric hyperoxia (1 atm ., 984 02) was found to be a very weak inducer of DNA
single-strand breaks and alkali-labile lesions, whereas H202 was found to induce large
amounts of strand breaks . Iron-chelators were unable to afford protection against the
clastogenic and SCE-inducing effects of hyperoxia, whereas it is known from the
literature that they do protect Chinese hamster cells against the induction of DNA
strand breaks and SCEs by H202 . From these results, together with the knowledge that
most OH radical-induced DNA lesions are detectable by alkaline elution, it is suggested
that the induction of genetic damage by hyperoxia is, in contrast to H202, probably
not OH radical mediated .
Data on the mutagenicity of hyperoxia and H202 on three loci (aprt, hprt, and
xprt) will be presented . Conclusions with respect to the type of mutation (base
substitutions and small deletions v .e . large deletions) induced by the different
sources of oxidative stress will be discussed .
Supported by grant 87-10 from the Netherlands Cancer Foundation .
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