Paraoxonase 1 activity, concentration and genotype in cardiovascular disease

Current Opinion in Lipidology

Volumn 15, Issue 4, 2004, Pages 399-404

  Mackness, Mike ^a   Durrington, Paul ^a   Mackness, Bharti ^a  

^a MANCHESTER ROYAL INFIRMARY   (United Kingdom)

Author keywords

Genetic polymorphism; High density lipoprotein; Oxidation; Paraoxonase 1

Indexed keywords

ACETYL HYDROLASE; ANTIOXIDANT; ARYLDIALKYLPHOSPHATASE; FIBRIC ACID DERIVATIVE; FLUINDOSTATIN; HIGH DENSITY LIPOPROTEIN; HOMOCYSTEINE; HYDROXYMETHYLGLUTARYL COENZYME A REDUCTASE INHIBITOR; PRAVASTATIN; SIMVASTATIN; THROMBOCYTE ACTIVATING FACTOR; UNCLASSIFIED DRUG;

ANTIOXIDANT ACTIVITY; CARDIOVASCULAR DISEASE; CARDIOVASCULAR RISK; CHEMICAL ANALYSIS; CONCENTRATION (PARAMETERS); CORONARY RISK; DRUG EFFECT; ENZYME ACTIVITY; ENZYME ANALYSIS; ENZYME MECHANISM; FOOD COMPOSITION; GENETIC EPIDEMIOLOGY; GENETIC POLYMORPHISM; GENOTYPE; HUMAN; ISCHEMIC HEART DISEASE; MEDICAL INFORMATION; METABOLISM; MOLECULAR BIOLOGY; NONHUMAN; NUTRITION; PRIORITY JOURNAL; PROSPECTIVE STUDY; PROTEIN FUNCTION; REGULATORY MECHANISM; REVIEW; RISK ASSESSMENT; RISK FACTOR;

1-ALKYL-2-ACETYLGLYCEROPHOSPHOCHOLINE ESTERASE; ANTIOXIDANTS; ARTERIOSCLEROSIS; ARYLDIALKYLPHOSPHATASE; CARDIOVASCULAR DISEASES; HOMOCYSTEINE; HUMANS; LIPOPROTEINS, HDL; MODELS, BIOLOGICAL; POLYMORPHISM, GENETIC;

EID: 4043096346     PISSN: 09579672     EISSN: None     Source Type: Journal    
DOI: 10.1097/01.mol.0000137227.54278.29     Document Type: Review

References (47)

1. Mackness MI, Arrol, S, Durrington PN. Paraoxonase prevents accumulation of lipoperoxides in low-density lipoprotein. FEBS Lett 1991; 286:152-154.
2. Mackness MI, Arrol S, Abbott CA, Durrington PN. Protection of low-density lipoprotein against oxidative modification by high-density lipoprotein associated paraoxonase. Atherosclerosis 1993; 104:129-135.
3. Watson AD, Berliner JA, Hama SY, et al. Protective effect of high density lipoprotein associated paraoxonase: inhibition of the biological activity of minimally oxidised low-density lipoprotein. J Clin Invest 1995; 96:2882-2891.
4. Ahmed Z, Ravandi A, Maguire GF, et al. Apolipoprotein A1 promotes the formation of phosphatidylcholine core aldehydes that are hydrolysed by paraoxonase (PON1) during high density lipoprotein oxidation with a peroxynitrite donor. J Biol Chem 2001; 276:24473-24481.
5. Aviram M, Rosenblat M, Bisgaier CL, et al. Paraoxonase inhibits high-density lipoprotein and preserves its functions. J Clin Invest 1998; 101:1581-1590.
6. Aviram M, Billecke S, Sorenson R, et al. Paraoxonase active site required for protection against LDL oxidation involves its free sulphydryl group and is different from that required for its arylesterase/paraoxonase activities: selective action of human paraoxonase alloenzymes Q and R. Arterioscl Thromb Vasc Biol 1998; 10:1617-1624.
7. Aviram M, Hardak E, Vaya J, et al. Human serum paraoxonase (PON1) Q and R selectively decrease lipid peroxides in human coronary and carotid atherosclerotic lesions: PON1 esterase and peroxidase-like activities. Circulation 2000; 101:2510-2517.
8. Mackness B, Durrington PN, Mackness MI. The paraoxonase gene family and coronary heart disease. Curr Opin Lipidol 2002; 13:357-362.
9. Mackness MI, Durrington PN, Mackness B. How HDL protects against the effects of lipid peroxidation. Curr Opin Lipidol 2000; 11:383-388.
10. Durrington PN, Mackness B, Mackness MI. Paraoxonase and atherosclerosis. Arterioscler Thromb Vasc Biol 2001; 21:473-480.
11. Rozenberg O, Rosenblat M, Coleman R, et al. Paraoxonase (PON1) deficiency is associated with increased macrophage oxidative stress: studies in PON1-knockout mice. Free Radic Biol Med 2003; 34:774-784. Provides an indication that PON1 in vivo can protect macrophages from oxidative stress, which may be a mechanism by which PON1 is antiatherogenic.
12. 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.
13. Robertson KS, Hawe E, Miller GJ, et al. Human paraoxonase gene cluster polymorphisms as predictors of coronary heart disease risk in the prospective Northwick Park Heart Study II. Biochim Biophys Acta 2003; 1639:203-212. The first prospective study of the association of PON gene polymorphisms with CHD indicating no associations except in the case of the L55M polymorphism and smokers.
14. Wheeler JG, Keavney B, Watkins H, et al. Four paraoxonse gene polymorphisms in 11,000 cases of coronary heart disease and 13,000 controls: meta-analysis of 43 studies. Lancet 2004; 363:689-695. This meta-analysis of the genetic-association studies published to date is important because it indicates that such studies do not provide any indication of the relevance of PON1 to atherosclerosis.
15. Abbott CA, Mackness MI, Kumar S, et al. Serum paraoxonase activity, concentration, and phenotype distribution in diabetes mellitus and its relationship to serum lipids and lipoproteins. Arterioscler Thromb Vasc Biol 1995; 15:1812-1818.
16. Mackness B, Durrington PN, Abuashia B, et al. Low paraoxonase activity in type II diabetes complicated by retinopathy. Clin Sci 2000; 98:355-363.
17. 55 genotype. Arterioscler Thromb Vasc Biol 2000; 20:2441-2447.
18. 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.
19. 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; 231:1465-1471. Another indication that PON1 activity rather than its genetic polymorphisms is associated with CHD development.
20. Mackness B, Durrington P, McElduff P, et al. Low paraoxonase activity predicts coronary events in the Caerphilly prospective study. Circulation 2003; 107:2775-2779. The first prospective study of the association of PON1 activity with CHD. Low PON1 activity was an independent risk factor for CHD.
21. Marathe GK, Zimmerman GA, McIntyre TM. Platelet-activating factor acetylhydrolase, and not paraoxonase-1, is the oxidized phospholipid hydrolase of high density lipoprotein particles. J Biol Chem 2003; 278:3937-3947.
22. Sorenson RC, Bisgaier CL, Aviram M, et al. Human serum Paraoxonase/Arylesterase's retained hydrophobic N-terminal leader sequence associates with HDLs by binding phospholipids: apolipoprotein A-I stabilizes activity. Arterioscler Thromb Vasc Biol 1999; 19:2214-2225.
23. Rodrigo L, Mackness B, Durrington PN, et al. Hydrolysis of platelet-activating factor by human serum paraoxonase. Biochem J 2001; 354:1-7.
24. Packard CJ, O'Reilly DSJ, Caslake MJ, et al. Lipoprotein-associated phospholipase A2 as an independent predictor of coronary heart disease. N Engl J Med 2000; 343:1148-1155.
25. Sangvanich P, Mackness B, Gaskill S, et al. The effect of HDL on the formation of lipid/protein conjugates during in vitro oxidation of LDL. Biochem Biophys Res Commun 2003; 300:501-506.
26. •].
27. Jarvik GP, Jampsa R, Richter RJ, et al. Novel paraoxonase (PON1) nonsense and missense mutations predicted by functional genomic assay of PON1 status. Pharmacogenetics 2003; 13:291-295. Two interesting papers describing previously unknown PON1 polymorphisms and their effect on activity.
28. 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. This paper is interesting mainly for the lack of the L55M polymorphism in the Han population.
29. Durrington PN, Mackness B, Mackness MI. The hunt for nutritional and pharmacological modulators of paraoxonase. Arterioscler Thromb Vasc Biol 2002; 22:1248-1250.
30. Ferré N, Camps J, Fernández-Ballart J, Arija V. Regulation of serum paraoxonase activity by genetic, nutritional, and lifestyle factors in the general population. Clin Chem 2003; 49:1491-1497. Article describing nongenetic factors affecting PON1 activity.
31. Jarvik GP, Tsai NT, McKinstry LA, et al. Vitamin C and E intake are associated with increased PON1 activity. Arterioscler Thromb Vasc Biol 2002; 22:1329-1333.
32. Vincent-Viry M, Sass C, Bastien S, et al. PON1-P192 phenotype and genotype assessments in 918 subjects of the Stanislas cohort study. Clin Chem Lab Med 2003; 41:535-540. Paper describing nongenetic factors affecting PON1 activity.
33. Seres I, Paragh G, Deschene E, et al. Study of factors influencing the decreased HDL associated PON1 activity with aging. Exp Gerontol 2004; 39:59-66.
34. Nguyen SD, Sok DE. Beneficial effect of oleoylated lipids on paraoxonase 1: protection against oxidative inactivation and stabilization. Biochem J 2003; 375:275-285. Oleoylated lipids protect PON1 from inactivation. Potentially important if this occurs in vivo.
35. •].
36. Sarandol E, Serdar Z, Dirican M, Safak O. Effects of red wine consumption on serum paraoxonase/arylesterase activities and on lipoprotein oxidizability in healthy-men. J Nutr Biochem 2003; 14:507-512. Two conflicting reports regarding the effect of alcohol consumption on PON1 activity.
37. Beltowski J, Wojcicka G, Jamroz A. Leptin decreases plasma paraoxonase 1 (PON1) activity and induces oxidative stress: the possible novel mechanism for proatherogenic effect of chronic hyperleptinemia. Atherosclerosis 2003; 170:21-29.
38. •].
39. •].
40. Gouédard C, Koum-Besson N, Barouki R, Morel Y. Opposite regulation of the human paraoxonase-1 gene PON1 by fenofibrate and statins. Mol Pharmacol 2003; 63:945-956. Three reports illustrating the confusion over the effects of lipid-lowering medication on PON1.
41. Wehner JM, Murphy-Erdosh C, Smolen A, Smolen TN. Genetic variation in paraoxonase activity and sensitivity to diisopropylphosphofluoridate in inbred mice. Pharmacol Biochem Behav 1987; 28:317-320.
42. Ali AB, Zhang Q, Lim YK, et al. Expression of major HDL-associated antioxidant PON1 is gender dependent and regulated during inflammation. Free Radic Biol Med 2003; 34:824-829.
43. Kumon Y, Suehiro T, Ikeda Y, Hashimoto K. Human paraoxonase-1 gene expression by HepG2 cells is downregulated by interleukin-1beta and tumor necrosis factor-alpha, but is upregulated by interleukin-6. Life Sci 2003; 73:2807-2815. These findings could provide a mechanistic link between inflammation, PON1 and atherosclerosis.
44. Robert K, Chasse JF, Santiard-Baron D, et al. Altered gene expression in liver from a murine model of hyperhomocysteinemia. J Biol Chem 2003; 278:31504-31511. This interesting article describes an inhibition of PON1 production in mice with hyperhomocysteinaemia which has interesting connotations in atherosclerosis development.
45. Jakubowski H. Calcium-dependent human serum homocysteine thiolactone hydrolase. J Biol Chem 2000; 275:3957-3962.
46. Ferretti G, Bacchetti T, Marotti E, Curatola G. Effect of homocysteinylation on human high-density lipoproteins: a correlation with paraoxonase activity. Metabolism 2003; 52:146-151.
47. Aviram M, Rosenblat M, Billecke S, et al. Human serum paraoxonase (PON1) is inactivated by oxidised low density lipoprotein and preserved by antioxidants. Free Radic Biol Med 1999; 26:892-904.