ASSOCIATION BETWEEN INHERITED THROMBOPHILIA
IN PREGNANCY AND MICRONUCLEUS FREQUENCY
IN PERIPHERAL BLOOD LYMPHOCYTES
Šošić GM1,*, Jović N2,5, Rakić B3, Dimitrijević A2,4, Varjačić M2,5
*Corresponding Author: Gordana M. Šošić, B.Sc., Department of Cytogenetic Diagnosis, Obstetrics and Gynecology
Clinic, Clinical Center “Kragujevac,” 30 Zmaj Jovina Street, 3400 Kragujevac, Serbia. Tel: +381-63-835-66-24.
Fax: +381-34-37-00-73. Email: gordana.sosic.2011.02@gmail.com
page: 11
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INTRODUCTION
During their lifetime, humans are exposed to exogenous
and endogenous agents who may react with cellular
biomolecules, especially with the DNA molecule and induce
changes in the genetic material that can lead to genomic
instability [1]. Micronucleus (MN) is a cytoplasmic
small nucleus containing particles of chromatin material
that is not incorporated into the nucleus of one of the daughter
cells during division. Under the influence of clastogenic
and aneugenic agents, micronuclei (MNi) are produced and
they may come from acentric chromatid/ chromosome fragments
or whole chromatids/chromosomes [1,2]. In health
biomonitoring, cytokinesis-block MN (CBMN) assay is
used to measure basal and induced chromosomal damage
in the peripheral blood lymphocytes (PBL) [2-3] and MN
frequency represents a quantitative indicator of structural
and/or numerical chromosomal aberrations [4-6].
The basal (spontaneous) MN frequency in PBL is a
measure of accumulated chromosomal aberrations occurring
during the lifetime of circulating lymphocytes [7].
The level of basal MN frequency is determined by the
contribution of genetic damage to the DNA that comes
from environmental factors and endogenous factors (genetic
and non genetic determinants) and the elimination
of DNA damage (that is determined by individual variations
in genes involved in DNA repair) [8]. The induced
MN frequency is the result of exposure to possible different
chemical, physical and biological mutagens and
carcinogens of natural or artificial origin [2-4]. Gender,
age, body weight, diet, life habits, presence of inflammation,
ionizing radiation and the use of certain medicines,
affect the increase of the MN frequency [9,10]. Higher MN
frequency in PBL is seen in persons with carcinoma [11],
neurodegenerative diseases [12], cardiovascular diseases
[13,14], autoimmune diseases [15], diabetes mellitus type 2 (T2DM) [16] and in persons with Down syndrome and
their parents [17]. For example, elevated MN frequency
is positively correlated with the occurrence and the severity
of coronary artery disease (CAD) [16,18]. It has
been reported that the TT genotype in the methylenetetrahydrofolate
reductase (MTHFR) C677T gene variant
is significantly associated with the higher MN in CAD
patients [5]. Genomic stability is essential for normal fetal
growth and development [19] and previous studies have
indicated the potential role of elevated MN in predicting
pregnancy complications in humans [20].
Thrombophilia presents a hereditary and acquired
hemostatic system disorder in which there is a tendency
towards thrombosis. During pregnancy, hypercoagulability
and hypofibrinolysis are present, which, together with
inherited and acquired thrombophilia conditions, can lead
to pregnancy complications [21]. A previous study has
shown the effectiveness of the treatment with low-molecular-
weight heparin (LMWH) on pregnancy outcomes in
women with thrombophilia [22].
There have been no clinical studies conducted to assess
the mutagenic potential of thrombophilia and complications
associated with this condition during pregnancy.
The aim of this study was to evaluate known risk factors,
to determine possible predictors of an increased frequency
of MN in PBL and the impact of thrombophilia on the
chromosomal instability in pregnant women in the first
trimester.
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