Environmental and Molecular Mutagenesis - Legacy Tobacco ...

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test,in vivo gnotQxicity test, we found th t GMA i eley tt ~{' the
sper. bner itY lreq p¢Y t e Qer . 1~ f∎i ~lasal~ P~3?2
~andoa~y ~~~ed ~ithiM an~ transere~ to np1~for ~~n~ orsat on .
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rhich terd through an~jt otrect g bas~ of ~aaase a~e~&s o luandsinCuce~ieet of terharor-ID4rlonel ~eD~ayr utesen
~ 647
aN ToXICITY AND t41fAMMITY OF CFDtCftII[M RICH BR6TaER's YEAST
Li Xili, Bai Cheng Jiang and Shen Juen, Div'n of Toxicology, Tianjin Medical College
Schwarz (1957) has postulated that trivalent chromium is an active eonstituent of
glueose tolerance factor (GTF) . Mertz (1969) denoted that animals with a deficiency
of trivalent chromium could result in damage of glucose tolerance or develop
diabetes, hyperlipemia and arteriosclerosis . The supplementation of chromium is
able to invert or prevent the pherxmena above mentioned . It is reported by China
Air Force Hospital that a supplesre .nt of 100mg/day of trivalent chraniunrrich yeast
to patients of diabetes and hyperlipemia induced an evident inprovecrent of glucose
tolerance and significant decrease of plasma lipids after several months . The
purpose of the present paper is to study the probably toxicity and nutagenicity of
of chrenium rich brewer's yeast . The results show that the W50 of chromium yeast
in rats and mice are all above 21 .5 g/kg, categorized as non-toxic and obtained
negative responses to micronucleus test, muse-sperm tmrptalogy test, Ames test
(TA98, 100, 97, 102), Reo-Assay, inductest and chromotest of SOS systan . We consider
it to be acceptable to use brewer's yeast as carrier of trivalent chromium
to be the source of chromium supplesnentation for certain populations deficient in
chromiun .
648 ,
TRANSPLACENTAL GENOTOXICITY OF TRIETHYLENEMELAMINE, BENZENE AND VINBLASTINE IN HICE .
S .C . Xing, X . Shi, Z-L . Wu, J-K . Chen, Z,Ona and W-Z . Whong, Division of Respiratory
Disease Studies, National Institute for Occupational Safety and Health, Morgantown,
WV (USA) A
Transplacental cytogenetic effects of triethylenemelamine (TEM), benzene and
vinblastine on maternal mice and their fetuses hsve been investigated in our
laboratory . CD1 mice of 12-14 days gestation were exposed to TEM, bensene and
vinblastine twice by intraperitoneal injection at a 24-h interval and sacrificed 40
hours after the first injection . Maternal bone marrow and fetal livers (2 to 4) from
each pregnant mouse were obtained for the micronucleus and the SCE analyses .
Significant dose-response increases in both micronucleus and SCE following the
treatment of TEM were found in maternal bone marrow and fetal liver cells . Benzene
at the highest dose (1 .5 ml/kg) also caused a significant increase in micronuclei and
SCEs in both maternal bone marrow and fetal liver cells . The data showed that the
embryonic genotoxic effect of TEM was much higher than that of benzene in both
genetic endpoints and that the frequency of micronucleus induced by benzene was
higher in fetal liver than in maternal bone marrow cells . Vinbiastine, a spindle
poisons agent, induced micronucleus formations but not SCEs . Micronucleus induction
by vinblastine was 7 folds greater in maternal bone marrow than in fetal liver
cells . All three chemicals showed cytotoxicity in maternal bone marrow cells, but
not in fetal liver cells except TEM, which showed a weak toxicity in fetal liver
cells in the micronucleus assay . These results indicate that TEM, bensene, and
vinblastine are transplacental genotoxicants in mice .
649
DELETION SCREENING AT THE CH ~cSE HAMS E hprt LOCUS USING THE POL -
MERASE C~AIN REACTION2 7~ . Xu~I , Y . Yu~~~, A .W . Hsiel, C .T . Caskey , B .
Rossiter , R .A . Gibbs I . Department of Preventive Medicine and
CommuTity Health, The University of Texas Medical Branch, Galveston2 TX
77550 Institute of Molecular Genetics, Baylor College of Medicine ,
Laboratories for Genetic Services, Inc .,3 Houston, TX 77030 .
We have developed a rapid screening method using the polymerase chain
reaction (PCR) for detecting deletions at the hypoxanthine-guanine
phosphoribosyltransferase (hprt) locus in Chinese hamster cells, CHO-K1-
BH4 and V79 . DNA was extracted from the HPRT-deficient mutants and two
primer sets were used to amplify 274-bp and 334-bp fragments containing
the exon 3 and exon 9 coding sequence, respectively . The PCR product was
directly analyzed by electrophoresis on agarose gels stained with
ethidium bromide . Using this assay, we analyzed 39 independently derived
HPRT mutants . Four out of ten spontaneous mutants showed deletions at
http://legacy.library.ucsf.edu/tid/clb93d00/pdf
1989 EMS Abstracts 223
Notes