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EC number: 202-486-1
CAS number: 96-18-4
The present abstract to a poster presentation (Ito, 1996) reports the
analysis of mouse forestomach tumor tissues via PCR. DNA was isolated
from paraffin-embedded tumor sections (obtained from the forestomach of
mice of the NTP bioassay on 1,2,3-trichloropropane, see chapter 7.7),
amplified by polymerase chain reaction, and analyzed by direct
sequencing for mutations in the ras-genes.
10 of 16 analysed tumors had a highly specific H-ras or K-ras mutation.
6 of the 10 had a H-ras mutation at codon 61 with 5 of the 6 showing a
AT to TA transversion in base 1. 4 of the 10 had a K-ras mutation at
codon 13 all of which showed a GC to CG transversion in base 1. These
transversions are most probably not caused by
S-[1-(hydroxymethyl)-2-(N7- guanypethyl]glutathione which is the major
DNA adduct that was found after 1,2,3-trichloropropane treatment.
Based on preliminary results that are not further specified in the
abstract, the authors propose that the found mutations are rather caused
through etheno DNA adducts (1,N6-ethenodeoxyadenosine and
3,N4-ethenodeoxycytidine) which stem from lipid peroxidation. The
proposed explanation is that the depletion of glutathion in cells that
are exposed to 1,2,3-trichloropropane causes an increase in lipid
peroxidation and thereby lead to the detrimental transversion mutations
that were found in the ras-genes.
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