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Study On The Association Of Paraoxonase 1 Gene T(-107)C And Paraoxonase 2 Gene C311S Polymorphisms With Serum Homocysteine Level And Serum Lipid And Coronary Heart Disease

Posted on:2006-07-25Degree:MasterType:Thesis
Country:ChinaCandidate:H WangFull Text:PDF
GTID:2144360155959485Subject:Department of Cardiology
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[Objective] To investigate the relationship between paraoxonase 1 (PON1) gene T(-107)C and paraoxonase 2 (PON2) gene C311S polymorphisms with serum homocysteine (Hey) level and serum lipids and coronary heart disease (CHD).[Methods] We addressed this issue in a case-control study in which 128 subjects with angiographically documented CHD and 280 subjects without CHD (excluded by coronarography). Serum Hey levels were detected with high-performance liquid chromatography (HPLC). Automated Biochemical Analyzer was used to measure the concentration of serum cholesterol (TC)> triglyceride (TG^ high density lipoprotein cholesterol (HDL-C) > low density lipoprotein cholesterol (LDL-C) and lipoprotein (a) (Lpa). Genomic DNA were extracted from the blood cell, polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) were used to detect the polymorphisms of PON 1 gene T(-107)C and PON2 gene C31 IS.[Results] (1) Compare the CHD patients with controls, the levels of serum Hcy> TC TG> Lpa â– > LDL-C were significant higher (PO.01) , the levels of serum HDL-C was significant lower in the former than those in the latter (P<0.05). (2)Through binary logistic regression analysis gender(male) ^ advanced age> hypertentions Hcy> LDL-C were confirmed to be risk factors for CHD and high level of HDL-C was a protective factor for CHD. Partial correlation analysis shows that the severity of coronary artery stenosis (the number of diseased vessels) was positively related to the levels of serum Hcy^ LDL-C and negatively to the HDL-Clevel (rHcy=0. 413, P<0. 01; rLDL-c=0. 175, P<0. 01; rm.^-0. 165, P<0. 01). (3) PON1T(-107)C polymorphism was not improved to be risk factors for CHD. The locus have two alleles (C and T) and three genetypes (CC> CI\ TT). No significant difference was found in the frequencies of genotypes and alleles of the polymorphisms between controls and CHD patients (P>0.05). Serum Hey level in CT/TT genetype was significant lower than that in CC genetype (P<0. 01). Serum lipids level were no significant difference (P>0.05). (4) PON2C31 IS polymorphism was not vertified to be risk factor for CHD. The locus have two alleles (C and S) and three genetypes (SS^ CS^ CC). No significant difference was found in the frequencies of genotypes and alleles of the polymorphisms between controls and CHD patients (P>0.05). The levels of the serum Hey and serum lipids were no significant difference in CS/CC genetype and SS genetype (P>0. 05). (5)Bettween lower Hey group (Hey^12.2Mmol/L) and higher Hey group (Hey > 12. 2Mmol/L), no significant difference was found in the frequencies of genotypes and alleles of the two sites polymorphisms (P>0. 05). (6) Bettween unstable angina patients and acute mycardiol infarction patients, bettween CHD and CHD+DM patients, the frequencies of genotypes and alleles and the levels of the serum Hey and serum lipids were no significant difference in the two polymorphisms (P>0.05). (7) The patients with -107C allel and 311C allel were susceptible to CHD. [Conclusion] (1) Gender(male^ advanced age ^ hypertntiom the high levels of serum Hey and LDL-C were risk factors for CHD and high level of HDL-C was a protective factor for CHD. The number of diseased coronary artery vessels was positively related to the levels of serum Hey and LDL-C and negatively to the HDL-C level. (2) PON1T(-107)C polymorphism was not a risk factor for CHD. But serum Hey level in CT/TT genetype was significant lower than that in CC genetype. That could be true that the PON1 activity were lower in CC genetype than that in CT/TT genetypes. CT/TT genotypes could be viewed as protective genotypes for CHD. (3) PON2C311S polymorphism was not a risk factor for CHD. It might...
Keywords/Search Tags:paraoxonase, coronary heart disease, gene polymorphism, serum homocysteine
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