Atherosclerosis
Volume 197, Issue 2 , Pages 556-563 , April 2008

Paraoxonase activity and coronary heart disease risk in healthy middle-aged males: The PRIME study

  • J.A. Troughton

      Affiliations

    • Faculty of Medicine, Queen's University Belfast, Belfast, Northern Ireland, UK
    • ,
  • J.V. Woodside

      Affiliations

    • Faculty of Medicine, Queen's University Belfast, Belfast, Northern Ireland, UK
    • Corresponding Author InformationCorresponding author at: Department of Medicine, Mulhouse Building, Grosvenor Road, Belfast BT12 6BJ, UK. Tel.: +44 28 90632585; fax: +44 28 90235900.
    • ,
  • J.W.G. Yarnell

      Affiliations

    • Faculty of Medicine, Queen's University Belfast, Belfast, Northern Ireland, UK
    • ,
  • D. Arveiler

      Affiliations

    • Strasbourg MONICA Project, Department of Epidemiology and Public Health, Faculty of Medicine, Strasbourg, France
    • ,
  • P. Amouyel

      Affiliations

    • Lille MONICA Project, INSERM U508, Pasteur Institute of Lille, Lille, France
    • ,
  • J. Ferrières

      Affiliations

    • Toulouse MONICA Project, INSERM U588, Department of Epidemiology, Paul Sabatier-Toulouse Purpan University, Toulouse, France
    • ,
  • P. Ducimetière

      Affiliations

    • Coordinating Center, INSERM U258, Hôpital Paul Brousse, Villejuif, France
    • ,
  • C.C. Patterson

      Affiliations

    • Faculty of Medicine, Queen's University Belfast, Belfast, Northern Ireland, UK
    • ,
  • G. Luc

      Affiliations

    • The Department of Atherosclerosis, INSERM U545, Institut Pasteur de Lille, Université de Lille 2, Lille, France
    • ,
  • on behalf of the PRIME Study Group

Received 10 April 2007 ,Revised 11 August 2007 ,Accepted 20 August 2007.

References 

  1. Ross R. The pathogenesis of atherosclerosis: a perspective for the 1990s. Nature. 1993;362:801–809
  2. Heller RF, Chinn S, Pedoe HD, Rose G. How well can we predict coronary heart disease? Findings in the United Kingdom Heart Disease Prevention Project. Br Med J (Clin Res Ed). 1984;288:1409–1411
  3. Yarnell JW. The PRIME study: classical risk factors do not explain the several fold differences in risk of coronary heart disease between France and Northern Ireland. Prospective Epidemiological Study of Myocardial Infarction. QJM. 1998;91:667–676
  4. Scarabin PY, Arveiler D, Amouyel P, et al. Plasma fibrinogen explains much of the difference in risk of coronary heart disease between France and Northern Ireland. The PRIME study. Atherosclerosis. 2003;166:103–109
  5. Blatter MC, James RW, Messmer S, Barja F, Pometta D. Identification of a distinct human high-density lipoprotein subspecies defined by a lipoprotein-associated protein, K-45. Identity of K-45 with paraoxonase. Eur J Biochem. 1993;211:871–879
  6. Adkins S, Gan KN, Mody M, La Du BN. Molecular basis for the polymorphic forms of human serum paraoxonase/arylesterase: glutamine or arginine at position 191, for the respective A or B allozymes. Am J Hum Genet. 1993;52:598–608
  7. Humbert R, Adler DA, Disteche CM, et al. The molecular basis of the human serum paraoxonase activity polymorphism. Nat Genet. 1993;3:73–76
  8. Mackness B, Mackness MI, Arrol S, Turkie W, Durrington PN. Effect of the molecular polymorphisms of human paraoxonase (PON1) on the rate of hydrolysis of paraoxon. Br J Pharmacol. 1997;122:265–268
  9. Mackness MI, Arrol S, Abbott C, Durrington PN. Protection of low-density lipoprotein against oxidative modification by high-density lipoprotein associated paraoxonase. Atherosclerosis. 1993;104:129–135
  10. Aviram M, Rosenblat M, Bisgaier CL, et al. Paraoxonase inhibits high-density lipoprotein oxidation and preserves its functions. A possible peroxidative role for paraoxonase. J Clin Invest. 1998;101:1581–1590
  11. Aviram M, Rosenblat M, Billecke S, et al. Human serum paraoxonase (PON 1) is inactivated by oxidized low density lipoprotein and preserved by antioxidants. Free Radic Biol Med. 1999;26:892–904
  12. Mackness B, Mackness MI, Arrol S, Turkie W, Durrington PN. Effect of the human serum paraoxonase 55 and 192 genetic polymorphisms on the protection by high density lipoprotein against low density lipoprotein oxidative modification. FEBS Lett. 1998;423:57–60
  13. Mackness B, Durrington P, McElduff P, et al. Low paraoxonase activity predicts coronary events in the Caerphilly Prospective Study. Circulation. 2003;107:2775–2779
  14. Mackness B, Mackness MI, Durrington PN, et al. Paraoxonase activity in two healthy populations with differing rates of coronary heart disease. Eur J Clin Invest. 2000;30:4–10
  15. Tunstall-Pedoe H, Kuulasmaa K, Amouyel P, et al. Myocardial infarction and coronary deaths in the World Health Organization MONICA Project. Registration procedures, event rates, and case-fatality rates in 38 populations from 21 countries in 4 continents. Circulation. 1994;90:583–612
  16. Ducimetiere P, Ruidavets JB, Montaye M, Haas B, Yarnell J. Five-year incidence of angina pectoris and other forms of coronary heart disease in healthy men aged 50–59 in France and Northern Ireland: the Prospective Epidemiological Study of Myocardial Infarction (PRIME) Study. Int J Epidemiol. 2001;30:1057–1062
  17. Rose GA, Blackburn H, Gillum RR, Prineas RJ. Cardiovascular survey methods. 2nd ed.. Geneva: World Health Organisation; 1982;
  18. Ortigoza-Ferado J, Richter RJ, Hornung SK, Motulsky AG, Furlong CE. Paraoxon hydrolysis in human serum mediated by a genetically variable arylesterase and albumin. Am J Hum Genet. 1984;36:295–305
  19. Gan KN, Smolen A, Eckerson HW, Ladu BN. Purification of human serum paraoxonase arylesterase—evidence for one esterase catalyzing both activities. Drug Metab Dispos. 1991;19:100–106
  20. Luc G, Bard JM, Ferrieres J, et al. Value of HDL cholesterol, apolipoprotein A-I, lipoprotein A-I, and lipoprotein A-I/A-II in prediction of coronary heart disease: the PRIME Study. Prospective Epidemiological Study of Myocardial Infarction. Arterioscler Thromb Vasc Biol. 2002;22:1155–1161
  21. Mackness B, Durrington P, Mackness M. Human serum paraoxonase. Gen Pharmacol. 1998;31(3):329–336
  22. Ayub A, Mackness MI, Arrol S, et al. Serum paraoxonase after myocardial infarction. Arterioscler Thromb Vasc Biol. 1999;19:330–335
  23. Mackness B, Davies GK, Turkie W, et al. Paraoxonase status in coronary heart disease: are activity and concentration more important than genotype?. Arterioscler Thromb Vasc Biol. 2001;21:1451–1457
  24. Wilson PW, D’Agostino RB, Levy D, et al. Prediction of coronary heart disease using risk factor categories. Circulation. 1998;97:1837–1847
  25. Ruiz J, Blanche H, James RW, et al. Gln-Arg192 polymorphism of paraoxonase and coronary heart disease in type 2 diabetes. Lancet. 1995;346:869–872
  26. Jarvik GP, Rozek LS, Brophy VH, et al. Paraoxonase (PON1) phenotype is a better predictor of vascular disease than is PON1(192) or PON1(55) genotype. Arterioscler Thromb Vasc Biol. 2000;20:2441–2447
  27. Horter MJ, Sondermann S, Reinecke H, et al. Associations of HDL phospholipids and paraoxonase activity with coronary heart disease in postmenopausal women. Acta Physiol Scand. 2002;176:123–130
  28. Karakaya A, Ibis S, Kural T, Kose SK, Karakaya AE. Serum paraoxonase activity and phenotype distribution in Turkish subjects with coronary heart disease and its relationship to serum lipids and lipoproteins. Chem Biol Interact. 1999;118:193–200
  29. Rahmani M, Raiszadeh F, Allahverdian S, et al. Coronary artery disease is associated with the ratio of apolipoprotein A-I/B and serum concentration of apolipoprotein B, but not with paraoxonase enzyme activity in Iranian subjects. Atherosclerosis. 2002;162:381–389
  30. Jarvik GP, Hatsukami TS, Carlson C, et al. Paraoxonase activity, but not haplotype utilizing the linkage disequilibrium structure, predicts vascular disease. Arterioscler Thromb Vasc Biol. 2003;23:1465–1471
  31. Brophy VH, Hastings MD, Clendenning JB, et al. Polymorphisms in the human paraoxonase (PON1) promoter. Pharmacogenetics. 2001;11:77–84
  32. Brophy VH, Jampsa RL, Clendenning JB, et al. Effects of 5′ regulatory-region polymorphisms on paraoxonase-gene (PON1) expression. Am J Hum Genet. 2001;68:1428–1436
  33. Leviev I, James RW. Promoter polymorphisms of human paraoxonase PON1 gene and serum paraoxonase activities and concentrations. Arterioscler Thromb Vasc Biol. 2000;20:516–521
  34. Suehiro T, Nakamura T, Inoue M, et al. A polymorphism upstream from the human paraoxonase (PON1) gene and its association with PON1 expression. Atherosclerosis. 2000;150:295–298
  35. Wang X, Fan Z, Huang J, et al. Extensive association analysis between polymorphisms of PON gene cluster with coronary heart disease in Chinese Han population. Arterioscler Thromb Vasc Biol. 2003;23:328–334
  36. James RW, Leviev I, Ruiz J, et al. Promoter polymorphism T(-107)C of the paraoxonase PON1 gene is a risk factor for coronary heart disease in type 2 diabetic patients. Diabetes. 2000;49:1390–1393
  37. Schmidt H, Schmidt R, Niederkorn K, et al. Paraoxonase PON1 polymorphism leu-Met54 is associated with carotid atherosclerosis: results of the Austrian Stroke Prevention Study. Stroke. 1998;29:2043–2048
  38. Malin R, Jarvinen O, Sisto T, Koivula T, Lehtimaki T. Paraoxonase producing PON1 gene M/L55 polymorphism is related to autopsy-verified artery-wall atherosclerosis. Atherosclerosis. 2001;157:301–307
  39. Fortunato G, Rubba P, Panico S, et al. A paraoxonase gene polymorphism, PON 1 (55), as an independent risk factor for increased carotid intima-media thickness in middle-aged women. Atherosclerosis. 2003;167:141–148
  40. Wheeler JG, Keavney BD, Watkins H, Collins R, Danesh J. Four paraoxonase gene polymorphisms in 11,212 cases of coronary heart disease and 12,786 controls: meta-analysis of 43 studies. Lancet. 2004;363:689–695
  41. Sanghera DK, Saha N, Kamboh MI. The codon 55 polymorphism in the paraoxonase 1 gene is not associated with the risk of coronary heart disease in Asian Indians and Chinese. Atherosclerosis. 1998;136:217–223

PII: S0021-9150(07)00529-1

doi: 10.1016/j.atherosclerosis.2007.08.019

Atherosclerosis
Volume 197, Issue 2 , Pages 556-563 , April 2008

Article Tools