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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

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