Pharmacological and dietary modulators of paraoxonase 1 (PON1) activity and expression: The hunt goes on

Costa, Lucio G.; Giordano, Gennaro; Furlong, Clement E.

doi:10.1016/j.bcp.2010.11.008

Cited by 170 publications

(134 citation statements)

References 98 publications

(140 reference statements)

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“…In the present study, administration of simvastatin evening or morning increased PON1 activity compared to baselines. Likewise, Costa et al (2011) reported that simvastatin treatment was increased PON1 activity. However, evening simvastatin administration caused significant increase in PON1 activity compared to morning dosing.…”

Section: Discussionmentioning

confidence: 95%

Influence of Simvastatin Chronotherapy on Erythrocytes Nitric oxide Synthase Activity

Harisa¹,

Alanazi²,

Attia³

et al. 2015

International J. of Pharmacology

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A B S T R A C TThis study was undertaken to investigate the impact simvastatin chronotherapy on erythrocytes Nitric Oxide Synthase (NOS) activity. In the present study we select 24 adult human subjects have plasma total cholesterol high borderline (200-230 mg dLG 1 ). Subjects were administrated simvastatin (20 mg day time) for 2 months. Afterward, they were recommended for washout period (2 weeks), then subjects were administered the same dose at night time for additional 2 months. The present results showed that both day time and night time simvastatin treatment regimen significantly decrease plasma atherogenic index, malondialdehyde and protein carbonyl levels. However, paraoxonase-1 activity and total thiol level were significantly increased. Moreover, simvastatin therapy improved nitrite (NO marker) levels in both plasma and erythrocytes compared to baselines. As well, simvastatin day time and night time dosing significantly increased erythrocytes NOS activity (46 and 64%, respectively) compared to baselines. Night time dosing induced marked increase of NOS activity (19%) compared to day time. This study confirms that night time dosing boost hypocholesterolemic, antioxidant and NO modulating effects of simvastatin compared to day time.

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Section: Discussionmentioning

confidence: 95%

Influence of Simvastatin Chronotherapy on Erythrocytes Nitric oxide Synthase Activity

Harisa¹,

Alanazi²,

Attia³

et al. 2015

International J. of Pharmacology

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“…Firstly, considering the factors that have been described to influence PON1 activity (for a review, see [44]) limitations of our study include lack of information on nutrition and alcohol consumption. Secondly, this is a cross-sectional study and therefore we cannot assert causality.…”

Section: Discussionmentioning

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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“…Moreover, a significant elevation in the plasma PON1 activity and the HDL-C level has been observed in hypercholesterolemic subjects, in response to anthocyanins at a dose of 160 mg two times daily [97]. It could not be excluded that substances with antioxidant potential -vitamin C and anthocyanins, but also polyphenols and vitamin E -prevent PON1 oxidation and in this way support the HDL-C functionality [18].…”

Section: Effect Of Diet On Paraoxonase 1 and Myeloperoxidase Activitiesmentioning

confidence: 99%

The contribution of paraoxonase 1 and myeloperoxidase to HDL-cholesterol functionality

Malara

Kęska

Lutosławska

2016

Biomedical Human Kinetics

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SummaryThe purpose of this study was to analyse the scientific evidence concerning the effects of two enzymes -paraoxonase 1 and myeloperoxidase -on the functions of HDL-cholesterol. It is well documented that disturbed circulating lipoproteins (a high total and high LDL-cholesterol, and low HDL-cholesterol) bring about atherosclerosis and an increased risk of cardiovascular disease (CVD) which is recognised as the main cause of death all around the world. In consequence, numerous studies have focused on procedures which will improve the plasma lipoproteins profile by decreasing the total cholesterol and the LDL-cholesterol (LDL-C) and increasing the HDL-cholesterol (HDL-C). However, the anti-atherogenic role of HDL-C has been challenged in studies showing that genetically elevated HDL-cholesterol does not offer protection against CVD. Moreover, it has been found that raising the circulating HDL-cholesterol fails to reduce atherosclerosis. The doubts concerning the protective role of HDL-C have been supported by in vitro studies which indicate that the HDL-C from patients with atherosclerosis does not have a protective action, but does stimulate inflammation and free radical synthesis. The above data suggests that HDL-C, commonly recognised as protective against atherosclerosis, in some circumstances becomes pro-atherogenic, and is thus dysfunctional. Our review focuses on two enzymes -paraoxonase 1 (PON1) and myeloperoxidase (MPO) -which markedly affect the properties of HDL-C and contribute to its anti -or pro-atherogenic activity. Moreover, the effects of the diet and physical activity on PON1 and MPO are summarised with respect to the HDL-C functionality.

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Pharmacological and dietary modulators of paraoxonase 1 (PON1) activity and expression: The hunt goes on

Cited by 170 publications

References 98 publications

Influence of Simvastatin Chronotherapy on Erythrocytes Nitric oxide Synthase Activity

Influence of Simvastatin Chronotherapy on Erythrocytes Nitric oxide Synthase Activity

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

The contribution of paraoxonase 1 and myeloperoxidase to HDL-cholesterol functionality

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