The Hunt for Nutritional and Pharmacological Modulators of Paraoxonase
2002; Lippincott Williams & Wilkins; Volume: 22; Issue: 8 Linguagem: Inglês
10.1161/01.atv.0000027414.34728.1f
ISSN1524-4636
AutoresPaul N. Durrington, Bharti Mackness, Mike Mackness,
Tópico(s)Biochemical Acid Research Studies
ResumoHomeArteriosclerosis, Thrombosis, and Vascular BiologyVol. 22, No. 8The Hunt for Nutritional and Pharmacological Modulators of Paraoxonase Free AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessEditorialPDF/EPUBThe Hunt for Nutritional and Pharmacological Modulators of Paraoxonase P.N. Durrington, B. Mackness and M.I. Mackness P.N. DurringtonP.N. Durrington From the University Department of Medicine, Manchester Royal Infirmary, Manchester, United Kingdom. , B. MacknessB. Mackness From the University Department of Medicine, Manchester Royal Infirmary, Manchester, United Kingdom. and M.I. MacknessM.I. Mackness From the University Department of Medicine, Manchester Royal Infirmary, Manchester, United Kingdom. Originally published1 Aug 2002https://doi.org/10.1161/01.ATV.0000027414.34728.1FArteriosclerosis, Thrombosis, and Vascular Biology. 2002;22:1248–1250Considerable experimental evidence suggests that lipid peroxides on LDL and their breakdown products are responsible for the physical changes in the LDL particle and the fragmentation of its apolipoprotein B, which permit it to bind to a wide range of high-affinity receptors on cells in the arterial wall, such as endothelial cells, macrophages, and smooth muscle cells, which are key players in atherosclerosis.1 Fat-soluble antioxidant vitamins in vitro delay the oxidation of LDL,2 suggesting that they might have the therapeutic potential to protect against coronary heart disease (CHD). However, now that several clinical trials of antioxidant fat-soluble vitamins have been completed, the reality is that they do not prevent coronary or other atherosclerotic events.2–4 The reasons for this have been reviewed,5 but germane to the issue may be that the protection against oxidation afforded to LDL by fat-soluble antioxidants is relatively short lived, being principally in the extension of the early lag phase in lipid peroxidation (conjugated diene formation) by a matter of minutes. They act as antioxidants only when they are more susceptible to oxidation than the molecules they protect, and once oxidized, they can become pro-oxidants.2 Additionally, erosion of their potential benefit may stem from their effect in increasing cholesteryl ester heteroexchange6,7 which is increasingly being viewed as proatherogenic.8–10 It could explain the amelioration by high-dose antioxidant vitamins of the regression of coronary atheroma induced by lipid-lowering drugs.11See page 1329Paraoxonase 1 (PON1), located on HDL, was first shown more than a decade ago to protect in vitro against the accumulation of lipid peroxides on LDL under oxidizing conditions .12 Unlike chain-breaking antioxidants, HDL prevents the accumulation of lipid peroxides on LDL13 and in the vessel wall14 for several hours, continuing to do so long after fat-soluble antioxidants have been exhausted, and this activity seems to be due to PON1.15–17 HDL is the predominant lipoprotein in tissue fluid, including cerebrospinal fluid and synovial fluid, and it is our hypothesis that HDL acts generally to prevent peroxidative damage to cell membranes (which LDL resembles) throughout the body.15,18 Indeed, HDL has been shown to protect erythrocyte membranes from peroxidative damage.19PON1 has been increasingly linked with atherosclerosis.20 There is an enormous 40-fold variation in the serum PON1 activity between individuals. Part of this variation is explained by polymorphisms of PON1 involving single amino acids at position 55 and 192 in its coding sequence.21 A lot of interest has focused on the association of these polymorphisms with CHD.20 The huge number of genetic studies result not so much from a more fundamental interest on the part of investigators in genes, but from the necessity to have stored serum as opposed to plasma to measure PON1 activity, which is highly calcium dependent. Although less intensively investigated, a much stronger association, however, exists between serum PON1 activity and CHD in case-control studies.22 Confirmation that PON1 influences the risk of atherosclerosis must come from clinical trials in which PON1 activity is raised nutritionally or pharmacologically. The report by Jarvik and colleagues23 in this issue of Arteriosclerosis, Thrombosis, and Vascular Biology is thus particularly interesting in the quest for modulators of PON1 activity. In this population study, the serum activity of PON1 was positively correlated with the (dietary and medicinal) intake of vitamins C and E and with statin treatment and inversely with smoking. One of the appeals of PON1 is that the antiatherogenic mechanism it offers could link LDL oxidation with atherogenesis despite the failure of antioxidant trials. If therefore, it turns out that antioxidant vitamins are themselves major determinants of PON1 activity, interest in PON1 could considerably diminish. However, the effect of vitamins C and E on PON1 activity observed by Jarvik et al23 is relatively small compared with overall individual variation in PON1 activity, and as they point out, it could be confounded because vitamin intake is also a marker for a generally healthier lifestyle. It must also be set against the possibly contradictory finding of an earlier investigation24 in which there was a negative correlation between serum PON1 activity and the intake of vegetables, presumably containing large amounts of vitamins C an E. None the less, Aviram and colleagues25 have previously shown in vitro that the antioxidant flavanoids quercetin and glabridin can protect PON1 in micellar solution (isolated from other HDL components) from loss of activity due to Cu2+-induced oxidation. This, however, is a highly artificial circumstance and Arrol and colleagues7 were unable to influence PON1 activity even with pharmacological doses of vitamin E given to volunteers. PON1 probably therefore does not require vitamin E for its activity, except perhaps in quantities present basally in the participants in their study.Jarvik et al23 also confirm earlier reports that smoking26 is an independent predictor of decreased PON1 activity. Although the effect of vitamins C and E persists after correction for smoking, higher dietary intake of vitamins is, however, likely to be associated with higher socioeconomic status and healthier nutritional and other lifestyles. High serum cholesterol27 and insulin resistance28 are, for example, associated with decreased PON1 activity. Studies of macronutrients in humans have not so far been undertaken, but in rodents, feeding monounsaturated fatty acids has been reported to lead to higher serum PON1 activity than saturated or highly polyunsaturated fatty acids.29 Degraded cooking oil30 and an atherogenic diet31,32 have also been reported to decrease PON1 activity in rabbits, mice, and humans. Polyphenols (present in wine, tea, and fruit juice) also increase PON1 activity in both humans and mice33 as does moderate alcohol intake.34 PON1 decreases in older people and with the beginning of menopause.35 Acute exposure to organophosphates decreases PON1 activity,36 but it is not certain yet whether chronic possible occupational low-level exposure to organophosphates or other toxins can influence PON1 activity.Thus it seems highly likely that nutritional and other environmental and occupational factors explain some of the individual variation in PON1 activity. These influences are likely to interact with the PON1 promoter polymorphisms recently described37 to produce further variation. Between populations, there are also marked differences in PON1 activity with populations of non-European origin having higher levels.21 In part, this is because the higher activity 192 polymorphic alleles are prevalent in people of African and Asian origin. However it is also likely that differences in nutrition and industrialization are critically important. Understandably, most of the interest in pharmacological effects on PON1 activity has thus far been in effects of lipid-lowering drugs. Some of these studies,38–40 but not all,41–43 suggest an effect of statins and fibrates in raising PON1 activity. The importance of further work in this area is that dietary or pharmacological interventions which will significantly increase PON1 activity may be discovered. These may prove to have application in the prevention of arteriosclerosis and make it possible to test the oxidant theory of atherosclerosis by an approach other than antioxidant vitamins.FootnotesCorrespondence to Dr P.N. Durrington, University Department of Medicine, Manchester Royal Infirmary, Oxford Road, Manchester M13 9WL, UK. E-mail [email protected] References 1 Lusis AJ. Atherosclerosis. Nature. 2000; 407: 233–241.CrossrefMedlineGoogle Scholar2 Stocker R. Dietary and pharmacological antioxidants in atherosclerosis. Curr Opin Lipidol. 1999; 10: 589–597.CrossrefMedlineGoogle Scholar3 Hennekens CH, Buring JE, Manson JE, Stampfer M, Rosner B, Cook NR, Belanger C, La Motte F, Gaziano JM, Ridker P, Willet W, Peto R. Lack of effect of long-term supplementation with beta carotene on the incidence of malignant neoplasms and cardiovascular disease. N Engl J Med. 1996; 334: 1145–1149.CrossrefMedlineGoogle Scholar4 The Heart Outcomes Prevention Evaluation Study Investigators. Vitamin E supplementation and cardiovascular events in high-risk patients. N Engl J Med. 2000; 342: 154–160.CrossrefMedlineGoogle Scholar5 Steinberg D. Is there a potential therapeutic role for vitamin E or other antioxidants in atherosclerosis? Curr Opin Lipidol. 2000; 11: 603–607.CrossrefMedlineGoogle Scholar6 Franceschini G, Chiesa G, Sirtori E. Probucol increases cholesteryl ester transfer protein activity in hypercholesterolaemic patients. Eur J Clin Invest. 1991; 21: 384–388.CrossrefMedlineGoogle Scholar7 Arrol S, Mackness MI, Durrington PN. Vitamin E supplementation increases the resistance of both LDL and HDL to oxidation and increases cholesteryl ester transfer activity. Atherosclerosis. 2000; 150: 129–134.CrossrefMedlineGoogle Scholar8 Barter P. CETP and atherosclerosis. Arterioscler Thromb Vasc Biol. 2000; 20: 2029–2031.CrossrefMedlineGoogle Scholar9 Rittershaus CW, Miller DP, Thomas LJ, Picard MD, Honan CM, Emmett CD, Pettey CL, Adari H, Hammond RA, Beattie DT, Callow AD, Marsh HC, Ryan US. Vaccine-induced antibodies inhibit CETP activity in vivo and reduce aortic lesion in a rabbit model of atherosclerosis. Arterioscler Thromb Vasc Biol. 2000; 20: 2106–2112.CrossrefMedlineGoogle Scholar10 Okamoto H, Yonemori F, Wakitani K, Minowa T, Maeda K, Shinkai H. A cholesteryl ester transfer protein inhibitor attenuates atherosclerosis in rabbits. Nature. 2000; 406: 203–207.CrossrefMedlineGoogle Scholar11 Brown BG, Zhao XQ, Chait A, Fisher LD, Cheung MC, Morse JS, Dowdy AA, Marino EK, Bolson EL, Alaupovic P, Frohlich J, Albers JJ. Simvastatin and niacin, antioxidant vitamins, or the combination for the prevention of coronary disease. N Engl J Med. 2001; 345: 1583–1592.CrossrefMedlineGoogle Scholar12 Mackness MI, Arrol S, Durrington PN. Paraoxonase prevents accumulation of lipoperoxides in low-density lipoprotein. FEBS Letts. 1991; 286: 152–154.CrossrefMedlineGoogle Scholar13 Mackness MI, Abbott CA, Arrol S, Durrington PN. The role of high-density lipoprotein and lipid-soluble antioxidant vitamins in inhibiting low-density lipoprotein oxidation. Biochem J. 1993; 294: 829–835.CrossrefMedlineGoogle Scholar14 Aviram M, Hardak E, Vaya J, Mahmood S, Milo S, Hoffmann A, Billicke S, Draganov D, Rosenblat M. 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.CrossrefMedlineGoogle Scholar15 Mackness MI, Arrol S, Abbott CA, and Durrington PN. Protection of low-density lipoprotein against oxidative modification by high-density lipoprotein associated paraoxonase. Atherosclerosis. 1993; 104: 129–135.CrossrefMedlineGoogle Scholar16 Shih DM, Gu L, Xia Y-R, Navab M, Li W-F, Hama S, Castellani LW, Furlong CE, Costa LG, Fogelman AM, Lusis AJ. Mice lacking serum paraoxonase are susceptible to organophosphate toxicity and atherosclerosis. Nature. 1998; 394: 284–287.CrossrefMedlineGoogle Scholar17 Mackness B, Durrington PN, Mackness MI. Lack of protection against oxidative modification of LDL by avian HDL. Biochem Biophys Res Comm. 1998; 247: 443–446.CrossrefMedlineGoogle Scholar18 Mackness MI, Mackness B, Arrol S, Wood G, Bhatnagar D, Durrington PN. Presence of paraoxonase in human interstitial fluid. FEBS Lett. 1997; 416: 377–380.CrossrefMedlineGoogle Scholar19 Klimov AN, Kozhevnikova KA, Kuzmin AA, Kuznetsov AS, Belova EV. On the ability of high density lipoproteins to remove phospholipid peroxidation products from erythrocyte membranes. Biochemistry (Moscow). 2001; 66: 300–304.CrossrefMedlineGoogle Scholar20 Durrington PN, Mackness B, Mackness MI. Paraoxonase and atherosclerosis. Arterioscler Thromb Vasc Biol. 2001; 21: 473–480.CrossrefMedlineGoogle Scholar21 Mackness B, Durrington PN, Mackness MI. Human serum paraoxonase. Gen Pharmacol. 1998; 31: 329–336.CrossrefMedlineGoogle Scholar22 Mackness B, Davies GK, Turkie W, Lee W, Roberts DH, Hill E, Roberts C, Durrington PN, Mackness MI. Paraoxonase status in coronary heart disease: are activity and concentration more important than genotype? Arterioscler Thromb Vasc Biol. 2001; 21: 1451–1457.CrossrefMedlineGoogle Scholar23 Jarvik GP, Tsai NT, McKinstry LA, Wani R, Brophy VH, Richter RJ, Schellenberg GD, Heagerty PJ, Hatsukami TS, Furlong CE. Vitamin C and E intake is associated with increased paraoxonase activity. Arterioscler Thromb Vasc Biol. 2002;221329–1333Google Scholar24 Kleemola P, Freese R, Jauhiainen M, Pahlman R, Alfthan G, Mutanen M. Dietary determinants of serum paraoxonase activity in healthy humans. Atheroslcerosis. 2002; 160: 425–432.CrossrefGoogle Scholar25 Aviram M, Rosenblat M, Billecke S, Erogul J, Sorenson R, Bisgaier CL, Newton RS, La Du BN. Human serum paraoxonase (PON1) is inactivated by oxidised low density lipoprotein and preserved by antioxidants. Free Radic Biol Med. 1999; 26: 892–904.CrossrefMedlineGoogle Scholar26 James RW, Leviev K, Righetti A. Smoking is associated with reduced serum paraoxonase activity and concentration in patients with coronary artery disease. Circulation. 2000; 101: 2252–2257.CrossrefMedlineGoogle Scholar27 Mackness MI, Harty D, Bhatnagar D, Winocour PH, Arrol S, Ishola M, Durrington PN. Serum paraoxonase activity in familial hypercholesterolaemia and insulin-dependent diabetes mellitus. Atherosclerosis. 1991; 86: 193–199.CrossrefMedlineGoogle Scholar28 Kordonouri O, James RW, Bennetts JB, Chan A, Kao YL, Danne T, Silink M, Donaghue K. Modulation by blood glucose levels of activity and concentration of paraoxonase in young patients with type 1 diabetes mellitus. Metabolism. 2001; 50: 657–660.CrossrefMedlineGoogle Scholar29 Kudchodkar BJ, Lacko AG, Dory L, Fungwe TV. Dietary fat modulates serum paraoxonase 1 activity in rats. J Nutr. 2000; 130: 2427–2433.CrossrefMedlineGoogle Scholar30 Sutherland WHF, Walker RJ, de Jong SA, van Rij AM, Phillips V, Walker HL. Reduced postprandial serum paraoxonase activity after a meal rich in used cooking fat. Arterioscler Thromb Vasc Biol. 1999; 19: 1340–1347.CrossrefMedlineGoogle Scholar31 Shih DM, Gu L, Hama S, Xia Y-R, Navab M, Fogelman AM, Lusis AJ. Genetic-dietary regulation of serum paraoxonase expression and its role in atherogenesis in a mouse model. J Clin Invest. 1996; 97: 1630–1639.CrossrefMedlineGoogle Scholar32 Mackness MI, Bouiller A, Hennuyer M, Mackness B, Hal M, Tailleux A, Duriez P, Delfly B, Durrington PN, Fruchart J-C, Duverger N, Caillaud J-M, Castro G. Paraoxonase activity is reduced by a pro-atherosclerotic diet in rabbits. Biochem Biophys Res Commun. 2000; 269: 232–236.CrossrefMedlineGoogle Scholar33 Aviram M, Dornfold L, Rosenblat M, Volkova N, Kaplan M, Coleman R, Hayek T, Presser D, Fuhrman B. Pomegranate juice consumption reduces oxidative stress, atherogenic modification of LDL, and platelet aggregation: studies in humans and in atherosclerotic apolipoprotein E-deficient mice. Am J Clin Nutr. 2000; 71: 1062–1076.CrossrefMedlineGoogle Scholar34 van der Gaag MS, van Tol A, Scheek LM, James RW, Urgert R, Schaafsma G, Hendriks HF. Daily moderate alcohol consumption increases serum paraoxonase activity: a diet controlled, randomised intervention study in middle-aged men. Atherosclerosis. 1999; 147: 405–410.CrossrefMedlineGoogle Scholar35 Senti M, Tomas M, Vila J, Marrugat J, Elosua R, Sala J, Masia R. Relationship of age-related myocardial infarction risk and Gln/Arg 192 variants of the human paraoxonase gene: the Regicor study. Atherosclerosis. 2001; 156: 443–449.CrossrefMedlineGoogle Scholar36 Sözmen EY, Mackness B, Sözmen B, Durrington P, Girgin FK, Aslan L, Mackness M. Effect of organophosphate intoxications on human serum paraoxonase. Hum Exp Toxicol. In press.Google Scholar37 Leviev I, James RW. Promoter polymorphisms of human paraoxonase PON1 gene and serum activities and concentrations. Arterioscler Thromb Vasc Biol. 2000; 20: 516–521.CrossrefMedlineGoogle Scholar38 Tomas M, Senti M, Garcia-Faria F, Vila J, Torrents A, Covas M, Marrugat J. Effect of simvastatin therapy on paraoxonase activity and related lipoproteins in familial hypercholesterolemic patients. Arterioscler Thromb Vasc Biol. 2000; 20: 2113–2119.CrossrefMedlineGoogle Scholar39 Aviram M, Rosenblat M, Bisgaier CL, Newton RS. Atorvastatin and gemfibrozil metabolites, but not the parent drugs are potent antioxidants against lipoprotein oxidation. Atherosclerosis. 1998; 138: 271–280.CrossrefMedlineGoogle Scholar40 Paragh G, Balogh Z, Seres I, Harangi M, Boda J, Kovacs P. Effect of gemfibrozil on HDL-associated serum paraoxonase activity and lipoprotein profile in patients with hyperlipidaemia. Clin Drug Invest. 2000;277–282.Google Scholar41 Durrington PN, Mackness MI, Bhatnagar D, Julier K, Prais H, Arrol S, Morgan J, Wood GNI. Effects of two different fibric acid derivatives on lipoproteins, cholesteryl ester transfer, fibrinogen, plasminogen activator inhibitor and paraoxonase activity in type IIb hyperlipoproteinaemia. Atherosclerosis. 1998; 138: 217–225.CrossrefMedlineGoogle Scholar42 Balogh Z, Fülöp P, Seres I, Harangi M, Katona E, Kovacs P, Kostaczky B, Paragh G. Effect of simvastatin on serum paraoxonase activity. Clin Drug Invest. 2001; 21: 505–510.CrossrefGoogle Scholar43 Turay J, Grniaková V, Valka J. Changes in paraoxonase and apolipoprotein A-I, B, C-III and E in subjects with combined familial hyperlipoproteinaemia treated with ciprofibrate. Drugs Exp Clin Res. 2000; 26: 83–88.MedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Longo A, Veiga G, Cousen M, Karpinski C, Schneider A, Weber B, Bertoldi E, Borges L and Bertacco R (2021)(2021) Factors associated to serum paraoxonase 1 activity in patients with cardiovascular disease, Archives of Endocrinology and Metabolism, 10.20945/2359-3997000000354, Online publication date: 12-Apr-2021., Online publication date: 12-Apr-2021. Grdić Rajković M, Popović-Grle S, Vukić Dugac A, Rogić D, Rako I, Radić Antolić M, Beriša M and Rumora L (2018) PON1 gene polymorphisms in patients with chronic obstructive pulmonary disease , Journal of Clinical Pathology, 10.1136/jclinpath-2018-205194, 71:11, (963-970), Online publication date: 1-Nov-2018. Meek E, Chambers H, Pringle R and Chambers J (2015) The effect of PON1 enhancers on reducing acetylcholinesterase inhibition following organophosphate anticholinesterase exposure in rats, Toxicology, 10.1016/j.tox.2015.08.002, 336, (79-83), Online publication date: 1-Oct-2015. Mackness M and Mackness B (2015) Human paraoxonase-1 (PON1): Gene structure and expression, promiscuous activities and multiple physiological roles, Gene, 10.1016/j.gene.2015.04.088, 567:1, (12-21), Online publication date: 1-Aug-2015. Gupta N, Kandimalla R, Priyanka K, Singh G, Gill K and Singh S (2013) Effect of Resveratrol and Nicotine on PON1 Gene Expression: In Vitro Study, Indian Journal of Clinical Biochemistry, 10.1007/s12291-013-0300-9, 29:1, (69-73), Online publication date: 1-Jan-2014. POSADAS-SÁNCHEZ R, POSADAS-ROMERO C, OCAMPO-ARCOS W, VILLARREAL-MOLINA M, VARGAS-ALARCÓN G, ANTÚNEZ-ARGÜELLES E, MENDOZA-PÉREZ E, CARDOSO-SALDAÑA G, MARTÍNEZ-ALVARADO R, MEDINA-URRUTIA A and JORGE-GALARZA E (2014)(2014) Premature and severe cardiovascular disease in a Mexican male with markedly low high-density-lipoprotein-cholesterol levels and a mutation in the lecithin:cholesterol acyltransferase gene: A family study, International Journal of Molecular Medicine, 10.3892/ijmm.2014.1733, 33:6, (1570-1576), Online publication date: 1-Jun-2014. Bernal-Hernández Y, Medina-Díaz I, Barrón-Vivanco B, Robledo-Marenco M, Girón-Pérez M, Pérez-Herrera N, Quintanilla-Vega B, Cerda-Flores R and Rojas-García A (2014) Paraoxonase 1 and Its Relationship With Pesticide Biomarkers in Indigenous Mexican Farmworkers, Journal of Occupational & Environmental Medicine, 10.1097/01.jom.0000438381.25597.88, 56:3, (281-290), Online publication date: 1-Mar-2014. Rumora L, Rajković M, Kopčinović L, Pancirov D, Čepelak I and Grubišić T (2014) Paraoxonase 1 Activity in Patients with Chronic Obstructive Pulmonary Disease, COPD: Journal of Chronic Obstructive Pulmonary Disease, 10.3109/15412555.2014.898028, 11:5, (539-545), Online publication date: 1-Sep-2014. Dansette P, Rosi J, Bertho G and Mansuy D (2011) Cytochromes P450 Catalyze Both Steps of the Major Pathway of Clopidogrel Bioactivation, whereas Paraoxonase Catalyzes the Formation of a Minor Thiol Metabolite Isomer, Chemical Research in Toxicology, 10.1021/tx2004085, 25:2, (348-356), Online publication date: 20-Feb-2012. Zhao Y, Ma Y, Fang Y, Liu L, Wu S, Fu D and Wang X (2012) Association between PON1 activity and coronary heart disease risk: A meta-analysis based on 43 studies, Molecular Genetics and Metabolism, 10.1016/j.ymgme.2011.09.018, 105:1, (141-148), Online publication date: 1-Jan-2012. Costa L, Giordano G and Furlong C (2011) Pharmacological and dietary modulators of paraoxonase 1 (PON1) activity and expression: The hunt goes on, Biochemical Pharmacology, 10.1016/j.bcp.2010.11.008, 81:3, (337-344), Online publication date: 1-Feb-2011. Mahrooz A, Rashidi M and Nouri M (2011) Naringenin is an inhibitor of human serum paraoxonase (PON1): an in vitro study, Journal of Clinical Laboratory Analysis, 10.1002/jcla.20490, 25:6, (395-401), Online publication date: 1-Nov-2011. Hofmann J, Keifer M, Checkoway H, De Roos A, Farin F, Fenske R, Richter R, van Belle G and Furlong C (2010) Biomarkers of Sensitivity and Exposure in Washington State Pesticide Handlers Paraoxonases in Inflammation, Infection, and Toxicology, 10.1007/978-1-60761-350-3_3, (19-27), . Samra Z, Shabir S, Rehmat Z, Zaman M, Nazir A, Dar N and Athar M (2009) Synthesis of Cholesterol-Conjugated Magnetic Nanoparticles for Purification of Human Paraoxonase 1, Applied Biochemistry and Biotechnology, 10.1007/s12010-009-8840-4, 162:3, (671-686), Online publication date: 1-Oct-2010. Hofmann J, Keifer M, Furlong C, De Roos A, Farin F, Fenske R, van Belle G and Checkoway H (2009) Serum Cholinesterase Inhibition in Relation to Paraoxonase-1 (PON1) Status among Organophosphate-Exposed Agricultural Pesticide Handlers, Environmental Health Perspectives, 10.1289/ehp.0900682, 117:9, (1402-1408), Online publication date: 1-Sep-2009. Jenkins A, Hill M and Rowley K (2008) Diabetes and Oxidant Stress Atherosclerosis and Oxidant Stress, 10.1007/978-0-387-72347-1_7, (123-158), . Dalgård C Dietary Modulation of Paraoxonase-1 Activity and Concentration in Humans The Paraoxonases: Their Role in Disease Development and Xenobiotic Metabolism, 10.1007/978-1-4020-6561-3_19, (283-293) Deakin S, Guernier S and James R (2007) Pharmacogenetic interaction between paraoxonase-1 gene promoter polymorphism C-107T and statin, Pharmacogenetics and Genomics, 10.1097/FPC.0b013e3280925716, 17:6, (451-457), Online publication date: 1-Jun-2007. Dalgård C, Christiansen L, Jonung T, Mackness M, de Maat M and Hørder M (2007) No influence of increased intake of orange and blackcurrant juices and dietary amounts of vitamin E on paraoxonase-1 activity in patients with peripheral arterial disease, European Journal of Nutrition, 10.1007/s00394-007-0675-6, 46:6, (354-363), Online publication date: 1-Sep-2007. Beer S, Moren X, Ruiz J and James R (2006) Postprandial modulation of serum paraoxonase activity and concentration in diabetic and non-diabetic subjects, Nutrition, Metabolism and Cardiovascular Diseases, 10.1016/j.numecd.2005.09.005, 16:7, (457-465), Online publication date: 1-Oct-2006. Kiss E, Soltesz P, Der H, Kocsis Z, Tarr T, Bhattoa H, Shoenfeld Y and Szegedi G (2006) Reduced flow-mediated vasodilation as a marker for cardiovascular complications in lupus patients, Journal of Autoimmunity, 10.1016/j.jaut.2006.09.008, 27:4, (211-217), Online publication date: 1-Dec-2006. Jung U, Lee M, Park Y, Kang M and Choi M (2006) Effect of citrus flavonoids on lipid metabolism and glucose-regulating enzyme mRNA levels in type-2 diabetic mice, The International Journal of Biochemistry & Cell Biology, 10.1016/j.biocel.2005.12.002, 38:7, (1134-1145), . Acín S, Navarro M, Carnicer R, Arbonés-Mainar J, Guzmán M, Arnal C, Beltrán G, Uceda M, Maeda N and Osada J (2005) Dietary cholesterol suppresses the ability of olive oil to delay the development of atherosclerotic lesions in apolipoprotein E knockout mice, Atherosclerosis, 10.1016/j.atherosclerosis.2005.01.050, 182:1, (17-28), Online publication date: 1-Sep-2005. Kopprasch S, Kreutzer F, Nowak V and Graessler J (2005) Intravenöse Sauerstofftherapie erhöht die Aktivität des antioxidativen und antiatherogenetischen Enzyms Paraoxonase-1 im Serum, Complementary Medicine Research, 10.1159/000089012, 12:6, (342-346), . Costa L, Vitalone A, Cole T and Furlong C (2005) Modulation of paraoxonase (PON1) activity, Biochemical Pharmacology, 10.1016/j.bcp.2004.08.027, 69:4, (541-550), Online publication date: 1-Feb-2005. Gouédard C, Barouki R and Morel Y (2004) Induction of the Paraoxonase-1 Gene Expression by Resveratrol, Arteriosclerosis, Thrombosis, and Vascular Biology, 24:12, (2378-2383), Online publication date: 1-Dec-2004. Rea I, McKeown P, McMaster D, Young I, Patterson C, Savage M, Belton C, Marchegiani F, Olivieri F, Bonafe M and Franceschi C (2004) Paraoxonase polymorphisms PON1 192 and 55 and longevity in Italian centenarians and Irish nonagenarians. A pooled analysis, Experimental Gerontology, 10.1016/j.exger.2003.11.019, 39:4, (629-635), Online publication date: 1-Apr-2004. Mackness B and Mackness M (2004) Paraoxonase 1: biochemistry and contribution to atherosclerosis, International Congress Series, 10.1016/S0531-5131(03)01736-9, 1262, (91-94), Online publication date: 1-May-2004. Gouédard C, Barouki R and Morel Y (2004) Dietary Polyphenols Increase Paraoxonase 1 Gene Expression by an Aryl Hydrocarbon Receptor-Dependent Mechanism, Molecular and Cellular Biology, 10.1128/MCB.24.12.5209-5222.2004, 24:12, (5209-5222), Online publication date: 15-Jun-2004. Mackness M, Durrington P and Mackness B (2004) Paraoxonase 1 activity, concentration and genotype in cardiovascular disease, Current Opinion in Lipidology, 10.1097/01.mol.0000137227.54278.29, 15:4, (399-404), Online publication date: 1-Aug-2004. Mackness B, Durrington P, McElduff P, Yarnell J, Azam N, Watt M and Mackness M (2003) Low Paraoxonase Activity Predicts Coronary Events in the Caerphilly Prospective Study, Circulation, 107:22, (2775-2779), Online publication date: 10-Jun-2003. Blatter-Garin M, Kalix B, De Pree S and James R (2003) Aspirin use is associated with higher serum concentrations of the anti-oxidant enzyme, paraoxonase-1, Diabetologia, 10.1007/s00125-003-1065-0, 46:4, (594-595), Online publication date: 1-Apr-2003. Ferré N, Camps J, Fernández-Ballart J, Arija V, Murphy M, Ceruelo S, Biarnés E, Vilella E, Tous M and Joven J (2003) Regulation of Serum Paraoxonase Activity by Genetic, Nutritional, and Lifestyle Factors in the General Population, Clinical Chemistry, 10.1373/49.9.1491, 49:9, (1491-1497), Online publication date: 1-Sep-2003. Vincent-Viry M, Sass C, Bastien S, Aguillon D, Siest G and Visvikis S PON1-192 Phenotype and Genotype Assessments in 918 Subjects of the Stanislas Cohort Study, Clinical Chemistry and Laboratory Medicine, 10.1515/CCLM.2003.081, 41:4 Navarro-García F, Ponce-Ruíz N, Rojas-García A, Ávila-Villarreal G, Herrera-Moreno J, Barrón-Vivanco B, Bernal-Hernández Y, González-Arias C and Medina-Díaz I (2021) The Role of Nutritional Habits and Moderate Red Wine Consumption in PON1 Status in Healthy Population, Applied Sciences, 10.3390/app11209503, 11:20, (9503) GÖKÇE B (2019) Bazı antrakinonların insan paraoksonaz 1 (hPON1) üzerine etkilerinin incelenmesi, Balıkesir Üniversitesi Fen Bilimleri Enstitüsü Dergisi, 10.25092/baunfbed.624457, (546-553) Juan J, Jiang X, Tang X, Wu Y, Sun K, Xiang X, Tian Y, Wu T, Sun Q, Kraft P and Hu Y (2017) Joint Effects of PON1 Polymorphisms and Vegetable Intake on Ischemic Stroke: A Family-Based Case Control Study, International Journal of Molecular Sciences, 10.3390/ijms18122652, 18:12, (2652) Lou-Bonafonte J, Gabás-Rivera C, Navarro M and Osada J (2015) PON1 and Mediterranean Diet, Nutrients, 10.3390/nu7064068, 7:6, (4068-4092) Rezaei N, Zaherijamil Z, Moradkhani S, Saidijam M, khodadadi I, Abbasi Oshaghi E and Tavilani H (2020) Kiwifruit Supplementation Increases the Activity of the Paraoxonase Enzyme and decreases Oxidized Low-Density Lipoprotein in High-Fat Diet Fed Hamsters, Avicenna Journal of Medical Biochemistry, 10.34172/ajmb.2020.09, 8:2, (58-63) August 2002Vol 22, Issue 8 Advertisement Article InformationMetrics https://doi.org/10.1161/01.ATV.0000027414.34728.1FPMID: 12171781 Originally publishedAugust 1, 2002 PDF download Advertisement
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