Environmental and Molecular Mutagenesis - Legacy Tobacco ...

6 1989 EMS Abstracts
Notes GENETIC TOXICOLOGY OF FOOD PRODUCTS
H .U . Aeschbacher, Nestld Research Centre, Nestec Ltd .
Lausanne 26 (Switzerland) .
http://legacy.library.ucsf.edu/tid/clb93d00/pdf
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Vers-chez-les-Blanc CH-1000
There is evidence from epidemiological studies that food is involved in cancer
etiology . Such a relationship has not generally been established for non
carcinogenic .genotoxic food components . This might be due in part to the difficulty to
provide evidence for genetic defects in man but might also be due to the fact that a
variety of food components which are positive In vitro are not harmful to man .
For instance, a number of compounds such as some vitamins, plant phenolics, etc are
mutagenic in vitro due to their antioxidant activity but might as a matter of fact
protect man from cancer . Food components also affect other mechanisms e .g . adsorption
to fiber, alteration of gut flora, etc, which can hardly be taken into account by In
vitro test systems .
It is therefore essential to permit for a correct risk assessment to thoroughly
investigate food-borne compounds with possible mutagenic or carcinogenic potential .
SYNEYISTIC GENOTOXF EFFECT OF.3 SMOKING AtiD LEAD. YR Ahulal, Talitha T
RaJah , B DineshKumar , NV Prasad , K Kashyap , K Krishnaswamy . 1)Dept . of
Genetics, Osmania University,2)National Institute of Nutrition 3)Govt Printing Press
4)Bureau of Polic . R6D, Hyderabad, INDIA .
Both smoking (S) and lead (Pb) have been shown to be genotoxic when tested
alone . Since the results of the studies on the Interacting effects between S and
Pb exposure are controversial, the present stud y was undertaken . Eighteen adult
male workers (8 of whom were smokers) exposed to Pb In a printing press and
25 controls were included in our study . Blood Pb levels were determined in 15
of the exposV subjects . Atmospheric Pb levels were also determined . Atmospheric
Pb (3 .1qjig/m ) was significantly higher as compared to the unpolluted environment
(0 .5ug/m ) . Blood Pb level was also significantly elevated (41 .55i5 .91,ug/dl) as
compared to controls (23 .6:3 .29,ug/dl) . Chromosome aberrations (CA) (structural+
numerical) were increased significantly in those who were exposed to Pb (15 .78%)
as compared to controls (6 .7%) . Amongst the Pb exposed workers, there was no
difference in the frequency of CA between smokers and nonsmokers (14 .16 vs
14 .70%)i however smokers had a significantly higher frequency of micronuclei
than nonsmokers (0 .85 vs 0 .44%) suggesting that 8 In combination with Pb is
clastogenic leading to cell death . The mitotic Index was also depressed in Pb
exposed smokers indicating that Pb In combination with smoking is cytotoxic .
Our results suggest that smoking interacts synergistically with Pb in causing genetic
damage .
Financial Assistance from ICMR is acknowledged .
NUCLEOID SEDIMENTATION ANALYSIS OF DNA DAMAGE PRODUCED BY NUTAGENS IN RAT LYMPHOCYTES .
Anane Aidoo, Ning Gao and Robert H . Heflich, National Center for Toxicological Research,
Jefferson, AR (USA), and Drug Inspection Institute of Inner Mongolia, Huhhot (PRC)
Assays based on detecting DNA damage in lymphocytes are used to monitor exposure to
potential genotoxic chemicals in vivo . In this study, we have examined the ability of
the model genotoxic agents, 2-acetylaminofluorene (2-AAF), benzo(a)pyrene (BP) and
several of their metabolites to produce DNA damage in rat lymphocytes . Lymphocytea,
isolated from the spleens of male Fischer 344 rats, were exposed to the agents for
one hour In serum-free medium . DNA damage was determined by the sedimentation rate of
nucleoids from the treated cells as compared with the appropriate controls . The
relative efficiency of producing DNA damage in rat lymphocytes by BP and its metabolites
was : BP anti-7,8-diol-9,10-epoxide > BP 4,5-oxide > BP trans-7,8-dihydrodiol a
BP, with the latter two compounds eliciting essentially no damage . For 2-AAF and its
derivatives, the order of potency was : N-acetoxy-2-AAF > N-hydroxy-2-aminofluorene
(N-hydroxy-2AF) a N-hydroxy-2-AAF > fluorene 3- 2-AF a 2-MF . The latter three compounds
produced very little damage . Paraoxon eliminated the DNA damage produced by Nacetoxy-2-AAF,
but both paraoxon and salicylamide had no affect on N-hydroxy-2-AAFinduced
damage . Rat lymphocytes also mediated a mutagenic response with N-hydroxy-
2-AAF in Salmonella ~t himuriu~m TA98 . These results indicate that rat lymphocyte
nucleoid seation detecS DNA damage produced by reactive metabolites of 2-AAF
and BP . While rat lymphocytes were capable of metabolizing N-acetoxy and N-hydroxy-
2-AAF to DNA-damaging species, they displayed little ability for activating the parent
compounds or BP trans-7,8-dihydrodiol .
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