ASSOCIATION BETWEEN INHERITED THROMBOPHILIA IN PREGNANCY AND MICRONUCLEUS FREQUENCY IN PERIPHERAL BLOOD LYMPHOCYTES
Šošić GM, Jović N2, Rakić B, Dimitrijević A, Varjačić M
*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
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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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