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Introduction

Metabolic syndrome ( MES ) is a collective of cardiovascular hazard factors, including high blood pressure, dyslipidemia, hyperglycaemia, and abdominal fleshiness. Resulting from the term ‘syndrome X ‘ suggested every bit early as 1988 by Reaven, MES is found to foretell development of type 2 diabetes mellitus ( T2DM ) and cardiovascular disease ( CVD ) in the hereafter. In add-on, MES has besides been reported to be linked with elevated serum high-sensitive C-reactive protein ( hsCRP ) , endothelial disfunction increased carotid intimamedia thickness ( IMT ) , and cardiovascular upset and mortality. MES has been defined by International Diabetes Federation ( IDF ) , American Heart Association and the National Heart, Lung, and Blood Institute ( AHA/NHLBI ) , National Cholesterol Education Program Adult Treatment Panal III ( NCEP-ATP III ) , and World Health Organization. Reports from different populations estimate the incidence of metabolic syndrome by each of the three definitions. 40 % of US grownups have MES by the IDF standards, which is higher than the prevalence defined by the ATPIII standards. IDF-defined MES is present in about half of the Grecian population. Sing, Iran population epidemiological informations on the prevalence of the metabolic syndrome are rare, most often used definitions for metabolic syndrome engage with different standards for diagnosing of fleshiness, hence fluctuation in the happening of metabolic syndrome seem to consequence the prevalence of adiposeness, the incidence of fleshiness has increased in the developing States such as Iran.

It is normally accepted that attempts to develop the apprehension of the familial function to complex diseases of babyhood will take to enhancement in the diagnosing and bar of such diseases. Many cistrons, including the human paraoxonase ( PON ) cistrons, have been implicated in development of complex disease such as Coronary bosom disease. The paraoxonase cistron household contains at least 3 members, including PON1, PON2 and PON3, which are located on chromosome 7q21.3-22.1. These cistrons portion significant structural homology and may hold derived from the tandem reproduction of a common evolutionary precursor.

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Human serum paraoxonase ( PON1. EC 3.1.8.1. ) , a 43-kDa protein, catalyses the hydrolysis of organophosphate esters, aromatic carboxylic acid esters, and carbonates. PON1 is synthesized in the liver and is chiefly related with high-density lipoprotein ( HDL ) . The enzyme lessenings assemblage of the lipid peroxides in low denseness lipoprotein ( LDL ) due to its ability to cut down hydro peroxides.

PON1 activity in human sera shows tremendous inter single fluctuation ( 40 fold ) as a consequence of familial and environmental factors, including environmental chemicals, pharmaceutical compounds, smoke, diet, intoxicant, and certain pathological and physiological conditions Familial factors include polymorphisms in the cryptography and booster parts of the pon1 cistron that might be influenced the PON1 look and its catalytic activity. Three common polymorphisms have been identified within PON1 cistron such as, Q192R glutamine to arginine permutation at place 192, L55M leucine to methionine permutation at place 55 and -108 C/T at booster part which affect PON1 activity towards paraoxon, diazoxon, GD and GB, it is linked with coronary arteria disease, shot, familial hypercholesteremia, type 2 diabetes and Parkinson ‘s disease.Therfore, L55M and-108C & gt ; T polymorphisms can impact its protein activity and messenger RNA degree, which might be concerned in shot, coronary arteria disease, Parkinson ‘s disease, change in plasma entire cholesterin and LDL cholesterin degrees. The purposes of this survey were to seek the of import function of Pon1 cistron polymorphism in the familial susceptibleness to MES and assay the distribution of pon1 SNPs ( Q192R, L55M and -108 C & gt ; T ) in healthy persons and patients with MES which diagnosed harmonizing to research lab trials in a Southeast Persian population.

Materials and methods

Subjects

The survey included 140 and 180 healthy unrelated persons and patients severally. This survey was performed from September 2008 to March 2009 in Zahedan, sou’-east, Iran. The survey was approved by the local ethical commission of Zahedan University of Medical Sciences and consented signifier was obtained from all topics. The following were collected by the research workers and a staff of medically trained voluntaries, demographic informations ( day of the month of birth, contact information, medical history, current medicines, household history, length of abode in the Zahedan ) ; height ( by a stadiometer utilizing a centimetre graduated table ) , weight ( by a clinical graduated table ) ; waist perimeter ( by a tape step merely upper the superior iliac crest with the topic standing, at the terminal of normal termination ) ; blood force per unit area ( by a quicksilver sphygmomanometer with the topic sitting ) ; and 5 milliliter of venous blood drained after 8-12 H fasting for research lab trials. Blood samples were collected by venopuncture after nightlong fasting. Blood collected in EDTA-coated tubing was used for finding of pon1 genotypes while sera were analyzed for Biochemical analysis ( fasting blood glucose, triglyceride, HDL-cholestrol ) was assayed utilizing a commercially available kit. Collected samples were stored at -20 A°C until analysis. Genomic DNA was isolated from EDTA-anticoagulated blood by a standard protease K digestion and phenol trichloromethane extraction method. The prevalence of metabolic syndrome among persons was determined harmonizing to IDF standards

Polymerase Chain Reaction ( PCR )

Polymorphisms were determined by the polymerase concatenation reaction followed by the elaboration furnace lining mutant system ( ARMS ) is a simple and rapid sensing method of point mutant and little nucleotide interpolation or omission.

The current survey, we used two tetra primer ARMS for the sensing of Q192R and L55M polymorphism as antecedently described and designed two outer primers ( frontward and change by reversal primer ) and two inner primers ( frontward and change by reversal ) for sensing fluctuations in -108 C & gt ; T cistron.

Statistical Analysis

The association between polymorphism in the Q 192R, L55M and -108C/T cistrons with the hazard of Metabolic syndrome was estimated by calculating odds ratio ( OR ) and 95 % assurance intervals ( 95 % CI ) , Categorical informations were tested utilizing Pearson ‘s x2. Multivariate logistic arrested development theoretical accounts were used to gauge adjusted odds ratio ( OR ) and 95 % assurance intervals ( 95 % CI ) .. Statistical analysis was performed utilizing SPSS version 10.0 ( SPSS, Chicago, IL ) and Epic version 3.2

Consequences:

One hundred 40 MES persons ( age 44.9+15.1 old ages ) and 183 controls ( age 34.7+13.5 old ages ) were successfully genotyped for the three PON1 polymorphisms. The corresponding genotype and allele frequences differed widely harmonizing to cognitive position. They were in Hardy-Weinberg equilibrium.

Pon1 genotypes and allelomorphs frequence were found to change between different cultural groups. When comparing Persian population with other population such as European and Asiatic, it has higher frequence of M allelomorph for L55M and C allele for-108C & gt ; T polymorphisms. In Asia Nipponese population shows predomination of R192 over Q192 allelomorphs and a really low frequence of M55 allelomorph.

Statistically, Significant association was found between patients with MES and RR genotype of PON1Q192R ( OR=2 ; 95 % CI, 1.17-3.40, P=0.001 ) . Therefore, the combined QR+RR genotype of Q192R cistron increased the hazard of metabolic syndrome significantly [ 1.62 ; 95 % CI, 1.0-2.63, p=0.05 ] .

The hazard in patients ( MES ) with MM and LM+MM genotypes of L54M cistron was in fringy boundary line ( OR ; 1.33 ; 95 % CI,068-1.85 ; p=0.73 and OR ; 1.12 ; 95 % CI,0.68-1.85, P=0.73 severally ) , In contrast, the CC genotype of 108C/T cistron was linked with a non significantly increased hazard of MES ( OR ; 1.61 ; 95 % CI,0.67-3.87 ) . In analysis of gene-gene interaction between Q192R and L55M cistrons, the magnitude of the association was greater with combined MM/RR genotypes [ OR=3.3 ( 1, 34-8.24 ) , p=0.007 ] . Even though in some combined genotypes OR was elevated up to put on the line degree, but, none of them had statistically important association with MES incidence.

Discussion:

Paraoxonases ( PONs ) i.e. PON1, PON2, PON3 are fundamentally lactonases. Of these, PON1 in add-on has an efficient esterase activity and can hydrolyse organophosphates. The PONs prevent low denseness lipoprotein cholesterin ( LDL-C ) from peroxidation, PON1 is entirely associated with high denseness lipoprotein cholesterin ( HDL-C ) and its antioxidant activity. Variations within PON1 cistron independently influence PON1 activity and have been defined as the molecular footing for interindividual variableness. These sites are designated as PON1 Q192R, L55M and -108 C & gt ; T which, the PON1 Q192R polymorphism appears to be the major determiner of the well known biochemical polymorphism in serum PON activity towards assorted organophosphates.

The frequences of the PON1 allelomorphs vary greatly across human populations. The distributions of two polymorphisms were significantly different between white and black adult females. The frequence of the PON1Met55 allelomorph was higher in white than inkinesss, whereas the frequence of the PON1 Arg192 allelomorph was contrary. The lowest frequence of the PON1 Met55 allelomorph had of all time been reported in Chinese, the comparatively high frequence of the PON1 Arg192 allelomorph in inkinesss is similar to that reported in Chinese and Nipponese, changing from 58 % to 65 % . The frequence of Q192R allelomorph in our survey was 54.7 % in instances and 68.40 % in controls which close to old study in Chinas and Nipponese population. However, Ferre et Al. have non found any important differences in genotype and allele frequences for PON1 polymorphisms at place 55 and 192 between healthy topics and patients with myocardial infarction in Spanish population. The frequences were similar to those described for other Caucasic populations. These disagreements may be related to the effects caused by other cistrons as PON2 or to posttranslational alterations of the enzymes.

The consequences presented here for a case-control survey indicate that bearers of the Arg allelomorph at place 192 of PON1 or topics with QR heterozygote for the booster polymorphism are at hazard of MES, this consequence is merely implicative of an impact of paraoxonase polymorphisms on the hazard of MES. Probe of gene-gene interaction between Q192R and L55M showed that the magnitude of the association was greater statistically with combined genotypes of MM/RR [ OR=3.3 ( 1,34-8.24 ) , p=0.007 ] , proposing that they functioned in combined mode.

Certain studies proposing a deficiency of association between paraoxonase polymorphism and AD or a protective consequence of the ArgArg genotype in Alzheimer ‘s disease ( AD ) . Helbecque et Al concluded that topics with TT heterozygote ( PON1 -108 C & gt ; T ) at the same time transporting an Arg allelomorph are at higher hazard of developing Eosinophilia-Myalgia Syndrome ( EMS ) . McGeachie et al. , ( 2009 ) reported a weak association of PON1 L55M with an increased hazard of wet Age-related Macular Degeneration ( AMD ) , their findings indicated a protective function for Gln192Arg, chiefly for patients with the wet signifier.

Sinha et Al. , ( 2009 ) suggested that there is a strong important correlativity between RR genotype of PON1Q192R and patients with Cardiovascular disease in North of India.The PON1-HDL composite may play a function in the homeostasis of coronary artery disease and HIV infection. Paragh and his co-workers hypothesized that arylesterase activity of PON1 would assist the formation of free-radical type arylamine derivates on the vesica epithelial surface, so that secondary metabolites of paraoxon or related chemicals and biotransformed intermediates of arylamines might be involved in formation of vesica carcinoma. Sing kidney disease, there was no important difference between patients and healthy groups in the frequence of PON1 polymorphisms ( L55M and Q 192 R ) . From this point of view, paraoxonase is a good campaigner cistron for analyzing involved hazard factors in MES development.

Decision, in the sou’-east Persian population, PON1 ( Q192R ) genotypes is significantly associated with increased hazard of MES. Therefore, it is possible that the comparative importance of PON1 as a hazard factor for MES here and other diseases might change in other populations because other gene-gene and gene-environment combinations are present. Therefore, it seems that the PON1 genotypes studied here do non to the full account for the variableness in PON1 metabolic capacity. Further analyses with larger sample size in different populations are needed to be clear uping the function of PON1 in the hazard of MES.

Recognitions: The writers thank the University of Sistan and Baluchistan-Zahedan, Iran, for financially back uping this undertaking under expansive 88G02. We are besides grateful to Zahedan University of medical scientific discipline, Zahedan Iran, for supplying us the Clinical samples.

Mention

  1. Hanley AJ, Karter AJ, Williams K, Festa A, D’Agostino RB Jr, Wagenknecht LE, Haffner SM. Prediction of type 2 diabetes mellitus with alternate definitions of the metabolic syndrome: the Insulin Resistance Atherosclerosis Study. Circulation. 2005 Dec 13 ; 112 ( 24 ) :3713-21.
  2. Sattar N, Gaw A, Scherbakova O, Ford I, O’Reilly DS, Haffner SM, et al. , Metabolic syndrome with and without Creactive protein as a forecaster of coronary bosom diseaseand diabetes in the West of Scotland Coronary Prevention Study. Circulation. 2003 ; 108:414.
  3. Reaven GM. Role of insulin opposition in human disease, Diabetes 1988 ; 37: 1595-1607.
  4. Ford ES. Risks for all-cause mortality, cardiovascular disease, and diabetes associated with the metabolic syndrome: a sum-up of the grounds, Diabetes Care 2005 ; 28: 1769-1778.
  5. Athyros VG, Ganotakis ES, Elisaf MS, Liberopoulos EN, Goudevenos IA, Karagiannis A ; GREECE-METS Collaborative Group. Prevalence of vascular disease in metabolic syndrome utilizing three proposed definitions.Int J Cardiol. 2007 Apr 25 ; 117 ( 2 ) :204-10.
  6. Rutter MK, Meigs JB, Sullivan LM, D’Agostino RB Sr, Wilson PW. C-reactive protein, the metabolic syndrome, and anticipation of cardiovascular events in the Framingham Offspring Study, Circulation. 2004 Jul 27 ; 110 ( 4 ) :380-5.
  7. Lteif AA, Han K, Mather KJ. Obesity, insulin opposition, and the metabolic syndrome: determiners of endothelial disfunction in Whites and inkinesss. Circulation. 2005 Jul 5 ; 112 ( 1 ) :32-8.
  8. Pollex RL, Al-Shali KZ, House AA, Spence JD, Fenster A, Mamakeesick M, Zinman B, Harris SB, Hanley AJ, Hegele RA. Relationship of the metabolic syndrome to carotid ultrasound traits, Cardiovasc Cardiovasc Ultrasound. 2006 Jul 7 ; 4:28.
  9. Isomaa B, Almgren P, Tuomi T, Forsen B, Lahti K, Nissen M, Taskinen MR, Groop L.Cardiovascular morbidity and mortality associated with the metabolic syndrome. Diabetes Care. 2001 Apr ; 24 ( 4 ) :683-9.
  10. Lee J, Heng D, Ma S, Chew SK, Hughes K, Tai ES. The metabolic syndrome and mortality: the Singapore Cardiovascular Cohort Study.Clin Endocrinol ( Oxf ) . 2008 Aug ; 69 ( 2 ) :225-30.
  11. Ma WY, Li HY, Hung CS, Lin MS, Chiu FC, Lin CH, Shih SR, Chuang LM, Wei JN. Metabolic syndrome defined by IDF and AHA/NHLBI correlates better to carotid intima-media thickness than that defined by NCEP ATP III and WHO. Diabetes Res Clin Pract. 2009 Sep ; 85 ( 3 ) :335-41.
  12. Wallenfeldt K, Hulthe J, Fagerberg B. The metabolic syndrome in middle-aged work forces harmonizing to different definitions and related alterations in carotid arteria intimamedia thickness ( IMT ) during 3 old ages of followup. J Intern Med. 2005 Jul ; 258 ( 1 ) :28-37.
  13. Lu B, Yang Y, Song X, Dong X, Zhang Z, Zhou L, Li Y, Zhao N, Zhu X, Hu R. An rating of the International Diabetes Federation definition of metabolic syndrome in Chinese patients older than 30 old ages and diagnosed with type 2 diabetes mellitus.Metabolism. 2006 Aug ; 55 ( 8 ) :1088-96.
  14. Lorenzo C, Serrano-Rios M, Martinez-Larrad MT, Gabriel R, Williams K, Gomez-Gerique JA, Stern MP, Haffner SM. Central adiposeness determines prevalence differences of the metabolic syndrome.Obes Res. 2003 Dec ; 11 ( 12 ) :1480-7
  15. Raymond SU, Leeder S, Greenberg HM. Obesity and cardiovascular disease in developing states: a turning job and an economic menace, Curr Opin Clin Nutr Metab Care.
  16. Prentice AM. , The emerging epidemic of fleshiness in developing states, Int. J. Epidemiol. 2006 ; 35:93-99.
  17. Azizi F, Azadbakht L, Mirmiran P.Trends in corpulence, fleshiness and cardinal fat accretion among Tehranian grownups between 1998-1999 and 2001-2002: Teheran lipoid and glucose survey, Ann. Nutr. Metab. 2005 ; 49: 3-8.
  18. Rashidi A, Mohammadpour-Ahranjani B, Vafa M. Karandish R M. Prevalence of fleshiness in Iran, Obes. Rev. 6 ( 2005 ) 191-192.
  19. Zabetian A, Hadaegh F, Azizi F.Prevalence of metabolic syndrome in Persian grownup population, harmony between the IDF with the ATPIII and the WHO definitions. Diabetes Research and Clinical Practice,2007 ; 77: 251-257
  20. Lander ES, Schork NJ. Genetic dissection of complex traits. Science 1994 ; 265:2037- 48.
  21. Schork NJ. Genetically Complex Cardiovascular Traits: Beginnings, Problems, and Potential Solutions Hypertension 1997 ; 29:145-9.
  22. Hegele RA. The familial footing of coronary artery disease. Int J Clin Lab Res 1997 ; 27:2- 13.
  23. Primo-Parmo SL, Sorenson RC, Teiber J, La Du BN. The human serum paraoxonase/arylesterase cistron ( PON1 ) is one member of a multigene household. Genomicss 1996 ; 33:498- 507.
  24. Mackness MI, Arrol S, Abbott CA, Durrington PN. Paraoxonase prevents accretion of lipoperoxides in low-density lipoprotein. FEBS Lett 1991 ; 286:152-4.
  25. Zhang Y, Zheng F, Du H, Krepinsky JC, Segbo JA, Zhou X..Detecting the polymorphisms of paraoxonase ( PON ) bunch in Chinese Han population based on a rapid method ) . Clin Chim Acta. 2006 Mar ; 365 ( 1-2 ) :98-103.
  26. Li B, Sedlacek M, Manoharan I, Boopathy R, Duysen EG, Masson P, Lockridge O. Butyrylcholinesterase, paraoxonase, and albumin esterase, but non carboxylesterase, are present in human plasma. Biochem Pharmacol. 2005 Nov 25 ; 70 ( 11 ) :1673-84.
  27. Tomas M, Latorre G, Senti M, Marrugat J. : The antioxidant map of high denseness lipoproteins: a new paradigm in coronary artery disease. Rev Esp Cardiol. 2004 Jun ; 57 ( 6 ) :557-69.
  28. Flekac M, Skrha J, Zidkova K, Lacinova Z, Hilgertova J.Paraoxonase 1 Gene Polymorphisms and Enzyme Activities in Diabetes Mellitus. Physiol Res. 2008 ; 57 ( 5 ) :717-26.
  29. Costa LG, Vitalone A, Cole TB, Furlong CE. Transition of paraoxonase ( PON1 ) activity. Biochem Pharmacol. 2005 Feb 15 ; 69 ( 4 ) :541-50.
  30. Leviev I, James RW. Promoter polymorphisms of human paraoxonase PON1 cistron and serum paraoxonase activities and concentrations. Arterioscler Thromb Vasc Biol. 2000 Feb ; 20 ( 2 ) :516-21.
  31. Durrington PN, Mackness B, Mackness MI. Paraoxonase and atherosclerosis. , Arterioscler Thromb Vasc Biol. 2001 Apr ; 21 ( 4 ) :473-80.
  32. Nga CJ, Diana B, Shiha M: The paraoxonase cistron household and coronary artery disease. Free Radic Biol Med 2005 ; 38: 153-163.
  33. Suehiro T, Nakamura T, Inoue M, Shiinoki T, Ikeda Y, Kumon Y, Shindo M, Tanaka H, Hashimoto K. A polymorphism upstream from the human paraoxonase ( PON1 ) cistron and its association with PON1 look. Atherosclerosis. 2000 Jun ; 150 ( 2 ) :295-8.
  34. Brophy VH, Hastings MD, Clendenning JB, Richter RJ, Jarvik GP, Furlong CE. Polymorphisms in the human paraoxonase ( PON1 ) booster. Pharmacogeneticss. 2001 Feb ; 11 ( 1 ) :77-84.
  35. Grdi M, BariK, RumoraL, SalamuniA TadijanoviM. Genetic Frequencies of Paraoxonase 1 Gene Polymorphisms in Croatian Population. CROATICA CHEMICA ACTA CCACAA. 2008 ; 81 ( 1 ) 105-111
  36. NewtonC R. Graham A and Heptinstall L E. Analysis of any point mutant in DNA. The elaboration furnace lining mutant ystem ( ARMS ) .Nucl.AcidsRes.1989a ; 17: 2503-2516.
  37. Ye S, Dhillon S, Ke X, Collins AR, Day IN.An efficient process for genotyping individual nucleotide polymorphisms. Nucleic Acids Res. 2001 Sep 1 ; 29 ( 17 ) : E88-8..
  38. Hashemi M, Moazeni-Roodi AK, Fazaeli A, Sandoughi M, Bardestani GR, Kordi-Tamandani DM, Ghavami S. Lack of association between paraoxonasae-1 Q192R polymorphism and arthritic arthritis in Southeast Iran Genitic and molecular research. Genet Mol Res. 2010 Feb 23 ; 9 ( 1 ) :333-9.
  39. Suehiro T, Nakamura T, Inoue M, Shiinoki T, Ikeda Y, Kumon Y, Shindo M, Tanaka H, Hashimoto K. A polymorphism upstream from the human paraoxonase ( PON1 ) cistron and its association with PON1 look. Atherosclerosis. 2000 Jun ; 150 ( 2 ) :295-8.
  40. Grdic, M. Barisic, K. Rumora, L. Salamunic, I. Tadijanovic, M. Grubisic, T.Z. Psikalova, R. Flegar-Mestric, Z. Juretic, D. Genetic Frequencies of Paraoxonase 1 Gene Polymorphisms in Croatian Population. CROATICA CHEMICA ACTA. 2008 ; 81: 105-111.
  41. Aynacioglu A S ; Cascorbi I ; Mrozikiewicz P M ; Nacak M ; Tapanyigit E E ; Roots I. Paraoxonase 1 mutants in a Turkish population. Toxicology and applied pharmacology1999 ; 157 ( 3 ) :174-7.
  42. O’Leary KA, Edwards RJ, Town MM, Boobis AR. Genetic and other beginnings of fluctuation in the activity of serum paraoxonase/diazoxonase in worlds: effects for hazard from exposure to diazinon. Pharmacogenet Genomics. 2005 Jan ; 15 ( 1 ) :51-60.
  43. Sardo MA, Campo S, Bonaiuto M, Bonaiuto A, Saitta C, Trimarchi G, Castaldo M, Bitto A, Cinquegrani M, Saitta A. Antioxidant consequence of Lipitor is independent of PON1 cistron T ( -107 ) C, Q192R and L55M polymorphisms in hypercholesterolaemic patients. Curr Med Res Opin. 2005 May ; 21 ( 5 ) :777-84.
  44. Parra S, Alonso-Villaverde C, Coll B, Ferre N, Marsillach J, Aragones G, Mackness M, Mackness B, Masana L, Joven J, Camps J. Serum paraoxonase-1 activity and concentration are influenced by human immunodeficiency virus infection. Atherosclerosis. 2007 Sep ; 194 ( 1 ) :175-81.
  45. Leus FR, Zwart M, Kastelein JJ, Voorbij HA. PON2 cistron discrepancies are associated with clinical manifestations of cardiovascular disease in familial hypercholesteremia patients. Atherosclerosis. 2001 Feb 15 ; 154 ( 3 ) :641-9.
  46. Clarimon J, Eerola J, Hellstrom O, Tienari PJ, Singleton A. Paraoxonase 1 ( PON1 ) cistron polymorphisms and Parkinson ‘s disease in a Finnish population. , Neurosci Lett. 2004 Sep 2 ; 367 ( 2 ) :168-70.
  47. Gupta N, Gill K, Singh S. Paraoxonases: construction, cistron polymorphism & A ; function in coronary arteria disease. Indian J Med Res. 2009 Oct ; 130 ( 4 ) :361-8.
  48. Humbert R, Adler DA, Disteche CM, Hassett C, Omiecinski CJ, Furlong CE ( 1993 ) The molecular footing of the human serum paraoxonase activity polymorphism. Nat Genet 3:73-76
  49. Watson CE, Draganov DI, Billecke SS, Bisgaier CL, La Du BN ( 2001 ) Rabbits possess a serum paraoxonase polymorphism similar to the human Q192R. Pharmacogeneticss 11:123-134.
  50. Ahmed Z, Ravandi A, Maguire GF, Emili A, Draganov D, La Du BN, Kuksis A, Connelly PW Apolipoprotein A-I promotes the formation of phosphatidylcholine nucleus aldehydes that are hydrolyzed by paraoxonase ( PON-1 ) during high denseness lipoprotein oxidization with a peroxynitrite giver. J Biol Chem ( 2001 ) . 276:24473-24481
  51. Imai Y, Morita H, Kurihara H, Sugiyama T, Kato N, Ebihara, A, Hamada C, Kurihara Y, Shindo T, Oh-hashi Y, Yazaki Y Evidence for association between paraoxonase cistron polymorphisms and atherosclerotic diseases. Atherosclerosis ( 2000 ) 49:435-442.
  52. Ko YL, Ko YS, Wang SM, Hsu LA, Chang CJ, Chu PH, Cheng NJ, Chen WJ, Chiang CW, Lee YS.The Gln- Arg 191 polymorphism of the human paraoxonase cistron is non associated with the hazard of coronary artery disease among Chinese in Taiwan. Atherosclerosis. 1998 Dec ; 141 ( 2 ) :259-64.
  53. Ferre N, Tous M, Paul A, Zamora A, Vendrell JJ, Bardaji A, Camps J, Richart C, Joven J Paraoxonase Gln-Arg ( 192 ) and Leu-Met ( 55 ) cistron polymorphisms and enzyme activity in a population with a low rate of coronary bosom disease. Clin Biochem 2002 ; 35:197-203
  54. Van Lenten BJ, Wagner AC, Navab M, Fogelman AM Oxidized phospholipids induce alterations in hepatic paraoxonase and ApoJ but non monocyte chemoattractant protein-1 via interleukin-6. J Biol Chem. 2001 ; 276:1923-1929
  55. Pola R, Gaetani E, Flex A, Gerardino L, Aloi F, Flore R, Serricchio M, Pola P, Bernabei R. Lack of association between Alzheimer ‘s disease and Gln-Arg 192 Q/R polymorphism of the PON-1 cistron in an Italian population Dement Geriatr Cogn Disord. 2003 ; 15 ( 2 ) :88-91.
  56. Scacchi R, Gambina G, Martini MC, Broggio E, Vilardo T, Corbo RM. Different form of association of paraoxonase Gln192 — & gt ; Arg polymorphism with sporadic late-onset Alzheimer ‘s disease and coronary arteria disease. Neurosci Lett. 2003 Mar 13 ; 339 ( 1 ) :17-20.
  57. Sodeyama N, Yamada M, Itoh Y, Suematsu N, Matsushita M, Otomo E, Mizusawa H. No association of paraoxonase cistron polymorphism with coronary artery disease or Alzheimer ‘s disease. Neurology. 1999 Sep 22 ; 53 ( 5 ) :1146-8.
  58. Helbecque N, Cottel D, Codron V, Berr C, Amouyel P. Paraoxonase 1 cistron polymorphisms and dementedness in worlds. Neurosci Lett. 2004 Mar 18 ; 358 ( 1 ) :41-4.
  59. Agrawal S, Tripathi G, Prajnya R, Sinha N, Gilmour A, Bush L, Mastana S. Paraoxonase 1 cistron polymorphisms contribute to coronary arteria disease hazard among north Indians. Indian J Med Sci. 2009 Aug ; 63 ( 8 ) :335-44
  60. Parra S, Marsillach J, Aragones G, Beltran R, Montero M, Coll B, Mackness B, Mackness M, Alonso-Villaverde C, Joven J, Camps J. Paraoxonase-1 cistron haplotypes are associated with metabolic perturbations, therosclerosis, and immunologic result in HIV-infected patients. J Infect Dis. 2010 Feb 15 ; 201 ( 4 ) :627-34.
  61. Ozturk O, Kagnici OF, Ozturk T, Durak H, Tuzuner BM, Kisakesen HI, Cakalir C, Isbir T. 192R allelomorph of paraoxanase 1 ( PON1 ) cistron as a new marker for susceptibleness to bladder malignant neoplastic disease. Anticancer Res. 2009 Oct ; 29 ( 10 ) :4041-6.
  62. Paragh G, Seres I, Harangi M, Pocsai Z, Asztalos L, Locsey L, Szeles G, Kardos L, Varga E, Karpati I, Adany R.Discordance in human paraoxonase-1 cistron between phenotypes and genotypes in chronic kidney disease. J Infect Dis. 2010 Feb 15 ; 201 ( 4 ) :627-34.

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