Environmental and Molecular Mutagenesis - Legacy Tobacco ...
Environmental and Molecular Mutagenesis - Legacy Tobacco ...
Environmental and Molecular Mutagenesis - Legacy Tobacco ...
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160 1989 EMS Abstracts<br />
http://legacy.library.ucsf.edu/tid/clb93d00/pdf<br />
463<br />
NULEES" "' °°''tYNERGISTIC-AL$qNReTOXICIIY OF ALCOH9L AND LB IN PRINTING PRESS 11ORKBRS .<br />
Talitha T Rajgh , NV Prasad , K Kashyap , YR AhuJeAq .1)Dept of Genetics, Osmania<br />
University . 2)C~,o_v~rlnting Press, 3)Bureau of Police . RBD, Hyderebad, INDIA .<br />
Lead (Pb) has been shown to have a mutagenic potential but reports on the<br />
mutagenicity of alcohol (A) are controversial . Since there are no reports available<br />
on the effect of Pb exposure in combination with A it was decided to study the<br />
cytogenetic effects of this combination . Air sampling was done to estimate the content<br />
of Pb In the working atmospherf~ The atmospheric Pb level was found to be elevited<br />
in the printing press (3 .144g/m ) as compared to the background value (0 .5A.g/m ) .<br />
Peripheral blood lymphocytes were cultured for 48 hrs from 20 adult males (10<br />
of whom were A consumers) working in a printing press . These individuals were<br />
exposed to Pb for more than 5 years . Twenty one healthy matched controls were<br />
also included . Chromosome aberrations (CA) were analysed from 100 metaphases<br />
per subject . A consumers did not show a significant increase in the frequency<br />
of CA (structual+numerical) as com pared to the control group (11 .35 vs 7 .54%) .<br />
But subjects exposed to Pb showed a significant increase In genotoxicity as compared<br />
to the controls (17 .60 vs 7 .54%) . When a comparison was made between alcohol<br />
consumers <strong>and</strong> nonconsumers within the Pb exposed group, there was a higher frequency<br />
of CA In the consumers than the nonconsumers (20 .72 vs 17 .60%) . This finding<br />
suggests that Pb <strong>and</strong> A interact In a synergistic manner In inducing genetic damage .<br />
Financial Assistance from ICMR Ss acknowledged .<br />
464<br />
MODULATION OF GENOTOXICITY, Claes Ramel, Department of Genetic <strong>and</strong> Cellular ToxicologK<br />
Wallenberg Laboratory, University of Stockholm, S-106 91 Stockholm, Sweden .<br />
In the absence of any principle breakthrough in cancer therapy, cancer prevention<br />
must rely on hindrance of induction of malignant growth . Chemoprevention of cancer by<br />
means of anticarcinogenic agents is one way towards this goal . This approach is favoured<br />
by the multistage process of carcinogenicity, where each step can be subjected<br />
to modulation by various agents . The critical role of genetic alterations In carcinogenicity,<br />
revealed by activation of oncogenes <strong>and</strong> inactivation of antioncogenes, focuses<br />
the attention on genotoxicity in this context . Modulation of genotoxicity can be<br />
achieved at two levels - by preventing chemical induction of mutations <strong>and</strong> by affecting<br />
the expression <strong>and</strong> regulation of altered genes . It has been shown that chemical<br />
induction of mutations can be modified by a large variety of chemicals acting at<br />
different levels - from the initial exposure to genotoxic chemicals to interactions<br />
with DNA <strong>and</strong> the establishment of mutations . The development of neoplasm comprise<br />
alterations of cellular messengers <strong>and</strong> interaction of gene products . The elucidation<br />
of this cellular signal system opens new prospects for chemoprevention of cancer by<br />
interference with the expression <strong>and</strong> regulation of genes involved In this system .<br />
UV-INDUCED TNYMIDINE INOORPORATION IN A CLINICAL VARIANT OF XERJDER4A PIGMENTOSW<br />
A . Shobha Rani . A . Jyothy, C.Kususe Kuearl, M . SuJetha, P.P .Raddy, <strong>and</strong> O .S.Rsddi.<br />
Institute of Geiwtics . Hoapital for Ganetie Diseasae, Ossenle Universitv . Beuumpet,HVderabad-S00 016 .<br />
A . P. Ind ia .<br />
ABSTRACT<br />
Xerodeima piymentosus Ss a rare autosoaal reaassive disease In which patients develop abnorael pigmentation<br />
<strong>and</strong> salipnancies !n the areas of the skin ezposed to sunlipht . These patients are unable to repair<br />
normally a certain type of UV induced daaape !n their DNA . The present lnvestl9etion is carried out<br />
to sae Sf there is any Japsinssnt in the repair process In this clinical variant with only occul .r senlfastation<br />
without any cutaneous manifestation .<br />
For the scintillation eeasurewent of raoelr . we used leukocvte ooouletions contelnina 1Xio cells . The<br />
cells vsre suspended In 1∎1 culture media with 205 serus . The cells were lrradiated with UV <strong>and</strong> then<br />
HTdR was added <strong>and</strong> reincubated for 24 hrs ., at 37oC. The cells rsre washed In saline followed by Sf <strong>and</strong><br />
10% TCA ( trichloroacatie acid) <strong>and</strong> finally In chilled es thenol . 0 .1 •1 of triton X-100 was added to<br />
dissolve the pellet <strong>and</strong> transferred to scintillation vials after which the activity was measured by<br />
B-counter . UV-induced thyaidlne incroporation rate 1s decreased to 20-37% In the affected individuels<br />
as compered to their unaffected sib (64%) parents ( 100% ) <strong>and</strong> controls (100f) lndicatin0 that ths<br />
rapair mechenis+. !n this clinical variant 1s Upaired .<br />
50869 3674<br />
465