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32
Songül Budak DİLER and Mehmet TOPAKTAŞ
Discussion
The sensitivity of human chromosomes to EMS
treatment was measured by determining the
breakages of each chromosome. In cultures treated
with different concentrations of EMS for 24 h and
48 h, the chromosomal breakage percentages were
statistically significant compared to control groups.
In addition, the percentage of fragmentation of each
chromosome at different concentrations of EMS
was significantly higher the controls. 24h EMS
treatment caused more fragmentation than 48h
treatment due to repair of damaged cells after 24h
treatment (Franke et al., 2006). Similar findings
also reported by several groups (Çakmak et al.,
2004, Rencüzoğulları et al., 2004, Bayram and
Topaktaş 2008).
In the control groups, chromosomes 1, 2, 6, X,
4 and 5 are susceptible to breakages to the first
degree. As can be seen, those chromosomes that are
tend to (natural) breakages in the control groups are
also susceptible to fragmentation in EMS-treated
cultures.
These results illustrate that the clastogens
cause more fragmentation of those chromosomes
that are prone to natural breakages. It has been
proposed that there may be a correlation between
the length of chromosomes and degree of
susceptibility to breakages. However, in this study,
in cultures treated with EMS, exception to this
assumption was discovered. For instance,
chromosome 3 fell into the second degree
susceptibility category in both untreated and EMS
treated cultures. This finding suggests that
chromosomal susceptibility to fragmentation may
correlate with its length as well as its composition.
Some investigators have discovered mutations
in some of the chromosomes derived from some
malignant cells, which we have found to be
sensitive to EMS treatment. The chromosomes we
found to be susceptible (chromosomes 1, 2, 3, 4, 5,
6, X, 7 and 8) were also found to be sensitive in
other studies. For instance, Bayani et al. showed by
spectral karyotyping that chromosomes 8, 7 and 20
were fragmented and rearranged in bone marrow
malignancies (Bayani et al.,2003). In cell lines
derived from stomach cancers, found that the p arm
of chromosome 17 showed partial deletion whilst
the q arm demonstrated partial duplication (Chun et
al., 2000). Selzer et al. studied neroblastomas and
their cell line derivatives, and discovered that there
was a loss in 3p and 11q whilst 17q showed
enlargement (Selzer et al., 2005). Gorunova et al.
showed that in gull bladder carcinomas,
chromosome 7 was the most frequently rearranged
one, followed by chromosomes 1, 3, 11, 6, 5 and 8.
(Gorunova et al., 1999). Morrissette et al.
discovered aberrations of chromosome 18 in
patients with partial mosaic tiresome (Morrissette et
al., 2005).
From these findings, it can be deduced that the
EMS test may prove to be indicative in some types
of cancer. Honma et al. compared the mutagenic
and cytotoxic response of the p53 tumor suppressor
gene in normal cells (TK6) and in cells with a
mutated p53 gene (WTK-1), both of which were
derived from he same ancestor. These two cell lines
were subjected to treatment with X-rays, EMS,
MMS and MMC. They found that the WTK-1 cells
were more resistant to induced cytotoxicity than the
TK6 cells, whiles their thymidine kinase (tk) gene
was more susceptible to mutation due to loss of
heterozygosity (LOH). These studies shows that
EMS can cause malignancies not only by the
cytogenetically specified chromosomal fragmentations
but also by alterations at the genetic level
(Honma et al., 1997).
In our study EMS caused chromosomal
breakages that are similar to the ones described by
these investigators. It can be argued that EMS may
constitute a risk factor in malignant transformations
due to its effect on chromosomal stability.
Acknowledgments
This study was supported by the C.U. Research
Fund. Project No. FBE2002D117.
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