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Environmental and Molecular Mutagenesis - Legacy Tobacco ...

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114 1989 EMS Abstracts<br />

Notes expzessed in quiescent calls . Enzyme induction may be a<br />

pleiotropic lnduetion effect on gene expraasions of the inducers .<br />

oNA methylation has been linked to alterations of gene<br />

expression . Induction of oncogene expression leads to the<br />

expression of aberrant oncogene products in "preinitiated" cells<br />

which are essential for their ultimate development into tumors .<br />

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

327<br />

1+iUTA(iENETIC EFFECT OF 15 C0IPOUNDS IN DROJOPHILA Al1BIIPI+OIDY '1S8TIACt .<br />

Li Hua1y1, Ca1 0on®min, Huang Jintang <strong>and</strong> Nan$ Zinmin, Department of<br />

Tozicoiogy, Second Military Medical Ooilege, 200433 8hanghai, P .R . CHINA<br />

In order to determine the sensitivity of Drosophila aneuploidy detecting<br />

syatem, the females (yw/yw) <strong>and</strong> the malea (yB/Yy) are used in our<br />

tests . The treatment sex male <strong>and</strong>/or lemale . The treatment stage lsrva<br />

<strong>and</strong>/or adult . The treatment route feeding method . The brood schedule of<br />

2-3-3 day broods ia carried out in all teats . Tested chemicals inoludes<br />

(1) Colcemid, (2) Colohioine, (3) Catieine, (4) Aotinomyoin D!( 5)Mett~yl<br />

methaneaullonate, (6) 5-Flurodeoxyuridine, (7) Proflavine, (8)0y0lophosphamide,<br />

(9) Mitomyoin-C, (10) Meprobamate (11) 8orbitor, (12)Urethane,<br />

(13) N-Methyl-N=nitroN-nitroaoguanidine, ~14) Sodium lluoride, (15) 5-<br />

Bromodeox}ruridine . Normal test described by Margolin et al (1983) are<br />

used in examine data for statistical aignifioanoe . The compounds which<br />

aignilicant difference at the 5% level between the treated <strong>and</strong> oontrol<br />

lrequencies of chromosome gain in treated d'inolude (1,2,5,7,9) <strong>and</strong> (3,<br />

4) in treated Q . The compounds which significant difference at the 5%<br />

level of chromosome loss in treated d inolude (4,6,7,8,9,11,12,13,14,15)<br />

<strong>and</strong> (1) in treated Q . U! 15 compounds tested for non-diajtimotion <strong>and</strong><br />

loas, only six (4,5,8,9 .12,13) have definitive oaroinogeneais olaaaif ication<br />

(a11 positive) . F ve (4 8,g,12,13) of these were significant di!lere<br />

oe for loas, three ~4 5 .9) o3 these rrere aignilioant di!lerence !or<br />

non-disjunction . Senaitivi~y ia 835: <strong>and</strong> 50>+, respectively.<br />

328<br />

MECHANISM OF ARSENITE INHIBITION OF REPAIR OF N-METHYL-N-NITROSOUREA-INDUCED DNA DAMAGE<br />

J .-H . Li <strong>and</strong> T.G . Rossman<br />

Institute of <strong>Environmental</strong> Medicine<br />

NYU Medical Center, NY, NY 10016<br />

Although inorganic arsenic compounds are known human carcinogens, they are not<br />

mutagens . The lack of arsenic mutagenicity has led us to study its comutagenicity .<br />

We have found that sodium arsenite at relatively nontoxic concentrations (5 uM for<br />

24 hours or 10 aM for 3 hours) is comutagenic with N-methyl-N-nitrosourea (MNU) at<br />

the hprt locus in Chinese hamster V79 cells . A nick translation assay, which measures<br />

DNA str<strong>and</strong> breaks in permeabilized cells, was utilized to show that str<strong>and</strong> breaks<br />

resulting from MNU or its repair accumulate in the presence of arsenite . MNU-induced<br />

poly (ADP-ribose) synthesis, measured by the incorporation of [3H]-NAD in the permeabilized<br />

cells, was also increased by post-treatment of the cells with araenite . This<br />

supports the hypothesis that arsenite inhibits the completion of DNA repair . The<br />

accumulated str<strong>and</strong> breaks in the presence of arsenite are probably not due to direct<br />

inhibition of DNA polymerase alpha, the presumed repair polymerase of MNU-induced DNA<br />

lesions, since very high concentrations of arsenite (about 7 .5 mM for 50% inhibition)<br />

are needed to inhibit this enzyme . We thus suggest that the repair of MNU-induced DNA<br />

lesions may be inhibited by arsenite by interfering with the ligation step .<br />

Supported by grant CA29258 from National Cancer Institute .<br />

GiNOlOIICMY Of ORCANIC gXIRAClS Q f3ggT foILS IN fICBI DIfZRIClS<br />

IN NgBo NANIN , pNILIppIlt3<br />

. .!s~ liaaoo . V . 1 . Isotiasds aad N . V . gotuysa , Iwtitute of<br />

stsy, o sge of Saiewoe, Uaiwrsity of tka pkilippias ., Dilioaa ,<br />

Quesoa City , pkilippiass<br />

Seventy-five per eeat of air pollutiee !a lMtro Naaila is ooatributed by<br />

emaissieas LrN sre tha 500,000 motor velioles operstiag daily . A awbsr of<br />

th.se vehicles are disssel powered vbiek oaa expose tlr urksa populatiea to<br />

diesel exlrusts wbiek eaatsia polyoyelie aresrtie Wreearkooa which posseas<br />

kvmaa eareimejaale poteatial . Tbase pelyeyelie aremetie Iqdreesr6elM esa<br />

aeeu .,late in street oils . orpaie extracts trem sieved soil Nmples trom<br />

lodustrial, oasrroial sad reaidsatisl areas ia eiakt distriets around Nstro<br />

Maaila - Nakati, Narikias, pasia, !sa Juaa, IMadaluyoaa, Csiata, Wleaswla<br />

<strong>and</strong> parsasque - were studied wlag tlr Rsa assay, bost-msdiated assay aad<br />

50g69 3626<br />

329

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