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Allelic polymorphism of endothelial No-synthase (eNOS) association with exercise-induced hypoxia adaptation

100%

Drozdovska S. B. , Dosenko V. E. , Ilyin V. N. , Filipov M. M. , Kuzmina S. B.

Baltic Journal of Health and Physical Activity. The Journal of Gdansk University of Physical Education and Sport

2009

tom 01

nr 1

The aim of the study is to define the possibility of usage of the gene eNOS polymorphisms as molecular-genetic markers of athletes’ resistance to exercise-induced hypoxia. 127 highly qualified athletes were examined (30 persons are underwater finswimmers, 41 - rowers and 56 sportsmen who practice speed and power track and field exercises). The frequency of promotor polymorphisms and the 7th exon of the eNOS gene in athletes engaged in finswimming and throwing has been studied. The comparative analysis of the obtained data with the frequency of allel variants of the eNOS gene has been carried out in athletes engaged in speed-power sports and the individuals not going in for sports. To study the influence of polymorphisms of this gene on individual values of resistance to hypoxia, a gas analysis was conducted in the athletes practicing rowing. During the study the eNOS gene expression was examined in athletes practicing short-course underwater finswimming with apneapracticing long distance swimming with a snorkel. The findings are evidence of a possible variant of influence of polymorphism of the eNOS gene on the phenotype formation resistant to exercise-induced hypoxia. Conclusions In the athletes practicing underwater finswimming, the occurrence of the allelic variant of C/C T786^C promoter polymorphism and T/T-variant in exon 7 of the gene of NO-synthase is lower than in the general population of Ukraine and in the athletes of speed and power type of sports, which may be the result of selection and be important for peculiarities of the development of resistance to exercise-induced hypoxia with different types of muscle activity.

Allelic polymorphism of endothelial NO-synthase gene and its functional manifestations

100%

Dosenko V. E. , Zagoriy V. Y. , Haytovich N. V. , Gordok O. A. , Moibenko A. A.

2006

tom 53

nr 2

Investigation of the mechanisms of phenotypic realization of allelic polymorphism of the eNOS gene has shown that the level of eNOS mRNA and activity of this enzyme in platelets depends from genotype. We identified a T-786→ C polymorphism in the promoter region, a variable number of tandem repeats (4a/4b) in intron 4 and the G894→ T polymorphism in exon 7 of the eNOS gene in isolated human platelets. We measured eNOS mRNA in isolated platelets by reverse transcription-PCR and eNOS enzyme activity by fluorimetric detection system FCANOS-1 using diaminofluorescein diacetate (DAF-2A). It was shown that the level of eNOS mRNA is the lowest for the -786C/C promoter genotype. In exon 7 homozygotes (894G/G) the level of RNA is lower than in normal homozygotes (894G/G), but higher than in heterozygotes (894G/T). The eNOS activity in platelets is lower in carriers of the 786C/C promoter genotype than in normal homozygotes (2.1 × P=0.03), and lower comparing to heterozygotes (2.9 × P > 0.05). The eNOS activity accompanying the 894G/G variant of exon 7 is also lower than in normal homozygotes (P > 0.05). Regarding the polymorphism in intron 4 - the enzyme's activity is lower in carriers of the 4a/4a genotype comparing to normal homozygotes (1.7 × P > 0.05) and lower than in heterozygotes (1.9 × P > 0.05). These results allow one to conclude that the G-786→ C polymorphism of the eNOS gene promoter most significantly affects the gene expression and eNOS activity.

Cardioprotective effect of 5-lipoxygenase gene [ALOX5] silencing in ischemia-reperfusion

86%

Lisovyy O. O. , Dosenko V. E. , Nagibin V. S. , Tumanovska L. V. , Korol M. O. , Surova O. V. , Moibenko O. O.

Acta Biochimica Polonica

2009

tom 56

nr 4

687-694

It is well known that 5-lipoxygenase derivates of arachidonic acid play an important pathogenic role during myocardial infarction. Therefore, the gene encoding arachidonate 5-lipoxygenase (ALOX5) appears to be an attractive target for RNA interference (RNAi) application. In experiments on cultivated cardiomyocytes with anoxia-reoxygenation (AR) and in vivo using rat model of heart ischemia-reperfusion (IR) we determined influence of ALOX5 silencing on myocardial cell death. ALOX5 silencing was quantified using real-time PCR, semi-quantitative PCR, and evaluation of LTC4 concentration in cardiac tissue. A 4.7-fold decrease of ALOX5 expression (P < 0.05) was observed in isolated cardiomyocytes together with a reduced number of necrotic cardiomyocytes (P < 0.05), increased number live (P < 0.05) and unchanged number of apoptotic cells during AR of cardiomyocytes. Downregulation of ALOX5 expression in myocardial tissue by 19% (P < 0.05) resulted in a 3.8-fold reduction of infarct size in an open chest rat model of heart IR (P < 0.05). Thus, RNAi targeting of ALOX5 protects heart cells against IR injury both in culture and in vivo.