The relationship between paraoxonase1-192 polymorphism and activity with coronary artery disease

Mohamed, Randa H.; Mohamed, Rasha H.; Karam, Rehab A.; El-Aziz, Tarek A. Abd

doi:10.1016/j.clinbiochem.2009.12.015

Cited by 45 publications

(24 citation statements)

References 42 publications

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“…R allozyme is less efficient at preventing the oxidation of LDL than the Q allozyme because of the decreased hydrolysis of lipid peroxides 13,14) . Hypothesized differences in the ability of the polymorphic forms to protect the oxidation of LDL have led to numerous studies attempting to determine the relationship between PON1 polymorphism and cardiovascular disease 4,13,[15][16][17][18][19][20][21][22][23][24][25][26] . These studies have yielded apparently conflicting results.…”

Section: Introductionmentioning

confidence: 99%

Serum PON-1 Activity but not Q192R Polymorphism is Related to the Extent of Atherosclerosis

Bayrak

Tokgözoğlu

et al. 2012

JAT

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Aim: Paraoxonase-1 (PON1) is an antioxidant enzyme located in high density lipoprotein (HDL). PON1 was defined as a protective factor against atherosclerosis. The aim of this study was to investigate the possible relationship between serum paraoxonase (PONase), homocysteine thiolactonase (HTase) activities and PON1 Q192R polymorphism, and the extent and severity of atherosclerosis. Methods: Blood specimens were collected from 142 individuals who had no coronary artery lesions angiographically (control group) and 128 individuals who had angiographically documented coronary artery disease of several degrees (patient group). The extent and severity of arterial lesions were evaluated by the Gensini scoring system. PONase and HTase activities were measured in serum using a spectrophotometric method. PON1 Q192R polymorphism was evaluated using PCR-RFLP after DNA isolation from blood. Results: Serum PONase and HTase activities were significantly lower in the patient group than in healthy controls (135.7 56.0 U/mL vs 153.8 62.0 U/mL, p 0.05; 36.0 6.1 U/mL vs 43.0 4.04 U/mL, p 0.01; respectively). In the patient group, there was a negative correlation between PONase, HTase activities and the Gensini score (r 0.168, p 0.039; r 0.164, p 0.006, respectively). In both groups, there was no significant difference in the distribution of PON1 Q192R polymorphism. In the patient group, the distribution of Gensini scores according to genotypes was not significant. Conclusion: It has been concluded that serum PONase and HTase activities might be a more relevant marker than PON1 genotype in evaluating the extent and severity of atherosclerosis.

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Section: Introductionmentioning

confidence: 99%

Serum PON-1 Activity but not Q192R Polymorphism is Related to the Extent of Atherosclerosis

Bayrak

Tokgözoğlu

et al. 2012

JAT

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“…Furthermore, it has been shown that reduced serum concentrations and the activity of PON1 in patients with coronary artery disease are related to the severity of the disease 6) . Along with various other diseases, low levels have also been reported in dialysis patients and are suggested as a contributor to atherosclerosis 24,25) . Changes in PON1 levels in renal transplant levels and how this affects the cardiovascular system are unclear.…”

Section: Discussionmentioning

confidence: 99%

Serum Paraoxonase 1 Activity Predicts Arterial Stiffness in Renal Transplant Recipients

Güngör

Kırçelli

Demirci

et al. 2011

JAT

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Aim: Paraoxanase 1 (PON 1) has been shown to protect against atherosclerosis by modifying lipoproteins. Its activity decreases in dialysis patients but is restored after transplantation. Whether it affects arterial stiffness is unclear. In this study we aimed to investigate the effects of PON 1 on arterial stiffness in renal transplant patients. Methods: Seventy renal transplant recipients were enrolled. Arterial stiffness was measured using a Syphmocor device. PON-1 activity was assessed from the rate of enzymatic hydrolysis of paraoxon to p-nitrophenol.

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“…the PON1-QR genotype increases the Framingham risk score and the interaction between smoking by PON1-RR carriers is associated with an increased AIP and Framingham score risk and by lowered HDLcholesterol and increased triglyceride levels. An atherogenic lipid profile and increased incidence of cardiovascular disease have been described in individuals homozygous to the PON1*192R allele (12,27,28). In a study performed on non-cardiovascular patients, PON1-RR smokers had a more atherogenic lipid profile (29).…”

Section: Discussionmentioning

confidence: 99%

“…The PON1 Q192R polymorphism determines in part PON1 hydrolytic activity and therefore plays a role in the protection of LDL and HDL against oxidation. These effects are, however, heavily debated since both the PON1*192Q allele (8)(9)(10) and the PON1*192R allele (11,12) have been associated with increased risk for cardiovascular disease, while there are also studies describing no association (13). One factor that may explain the contradictory results is the approach used to evaluate PON1.…”

Section: Introductionmentioning

confidence: 99%

Paraoxonase 1 (PON1) Q192R genotypes and their interaction with smoking strongly increase atherogenicity and the Framingham risk score

Souza-Nogueira

Camargo

Remondi

et al. 2016

Arch. Endocrinol. Metab.

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Objective: Paraoxonase 1 (PON1) polymorphisms are associated with an increased susceptibility to cardiovascular disease. PON1 Q192R polymorphism (rs662) partially determine PON1 hydrolytic activity and protect against oxidation of LDL and HDL. This study aimed to delineate the association of PON1 status (functional 192 genotype and plasma activity levels) and atherogenicity in urbans residents aged 40 years or more. Materials and methods: Anthropometric data, lipid profiles, the atherogenic index of the plasma (AIP) and Framingham score risk were measured. Three kinetic assays were conducted to assay PON1 status using phenylacetate and 4-(chloromethyl)phenyl acetate as substrates. Results: Smoking per se did not significantly impact the AIP but the interaction PON1 genotype by smoking significantly increased the AIP. In subjects with the RR genotype smoking increased the AIP index from (estimated mean ± SEM) -0.038 ± 0.039 to 0.224 ± 0.094. The QR genotype increased the Framingham risk index by around 1.3 points. Smoking by RR genotype carriers significantly increased the Framingham risk score (17.23 ± 2.04) as compared to smoking (13.00 ± 1.06) and non-smoking (7.79 ± 0.70) by QQ+QR genotype carriers. The interaction RR genotype by smoking was a more important predictor (odds ratio = 7.90) of an increased Framingham risk score (> 20) than smoking per se (odds ratio = 2.73). The interaction smoking by RR genotype carriers significantly increased triglycerides and lowered HDL cholesterol. Conclusion: Smoking per se has no (AIP) or a mild (Framingham risk score) effect on atherogenicity, while the interaction smoking by PON1 RR genotype has a clinically highly significant impact on atherogenicity. Arch Endocrinol Metab. 2016;60(5):426-35

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The relationship between paraoxonase1-192 polymorphism and activity with coronary artery disease

Cited by 45 publications

References 42 publications

Serum PON-1 Activity but not Q192R Polymorphism is Related to the Extent of Atherosclerosis

Serum PON-1 Activity but not Q192R Polymorphism is Related to the Extent of Atherosclerosis

Serum Paraoxonase 1 Activity Predicts Arterial Stiffness in Renal Transplant Recipients

Paraoxonase 1 (PON1) Q192R genotypes and their interaction with smoking strongly increase atherogenicity and the Framingham risk score

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