Paraoxonase gene polymorphisms and haplotype analysis in a stroke population

Pasdar, Alireza; Ross-Adams, Helen; Cumming, Alastair M.; Cheung, J.; Whalley, Lawrence J.; Clair, David St; MacLeod, Mary Joan

doi:10.1186/1471-2350-7-28

Cited by 45 publications

(49 citation statements)

References 42 publications

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“…The G/G genotype frequency in Adjaethnic group (10.0 %) was similar to that observed in Chinese Li minority (8.0 %), but was significant different from that observed inAdjaethnic group (19.0 %).There were also significant differences in PON3 Ala99Ala polymorphism distribution in Beninese AdjaandMahiethnic groups compared to British Caucasians (p<0.05) (Robertson, 2003;Pasdar, 2006). Additional studies on large cohorts from different ethnic groups in Benin may be needed to determine the real genotypes distribution of PON3 Ala99Ala polymorphism in Beninese population…”

Section: Discussion:-supporting

confidence: 54%

“…The expression of PON3 gene occurs mainly in the liver and bind to HDL in blood stream (Reddy et al, 2001). The PON3 gene has five commons Single Nucleotide Polymorphisms (SNPs) Ala99Ala, Asp107Asn, Glu146Lys, Ala179Asp and Tyr233Cys (Robertson et al, 2003;Li et al, 2004;Pasdar et al, 2006 andSanghera et al, 2008). Despite the importance of the paraoxonase gene and its implications on the genetic susceptibility to coronary heart disease, no studies on African black populations have been reported.…”

mentioning

confidence: 99%

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Genetic Polymorphism of Paraoxonase 3 Gene Ala99ala in Adjaandmahiethnic Groups in Benin.

Segbo.¹,

Houngnonvi.²,

Missihoun.³

et al. 2017

IJAR

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Section: Discussion:-supporting

confidence: 54%

mentioning

confidence: 99%

Genetic Polymorphism of Paraoxonase 3 Gene Ala99ala in Adjaandmahiethnic Groups in Benin.

Segbo.¹,

Houngnonvi.²,

Missihoun.³

et al. 2017

IJAR

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“…[49][50][51][52][53][54][55][56][57][58][59][60][61][62][63][64][65][66] Liu et al in 2013 conducted and published a systematic review and meta-analysis of 28 selected studies addressing these relationships. 21 They found that the R allele and the RR genotype of PON1 Q192R polymorphism correlated with a higher risk for ischemic stroke in the general population.…”

Section: Pon1 and Ischemic Strokementioning

confidence: 99%

Paraoxonase 1 in neurological disorders

Menini

Gugliucci

2013

Redox Report

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Paroxonase 1 displays multiple physiological activities that position it as a putative player in the pathogenesis of neurological disorders. Here we reviewed the literature focusing on the role of paraoxonase 1 (PON1) as a factor in the risk of stroke and the major neurodegenerative diseases. PON1 activity is reduced in stroke patients, which significantly correlates inversely with carotid and cerebral atherosclerosis. The presence of the R allele of the Q192R PON1 polymorphism seems to potentiate this risk for stroke. PON1 exerts peroxidase activities that may be important in neurodegenerative disorders associated with oxidative stress. PON1 is also a key detoxifier of organophosphates and organophosphate exposure has been linked to the development of neurological disorders in which acetylcholine plays a significant role. In Parkinson's disease most of the studies suggest no participation of either L55M or the Q192R polymorphisms in its pathogenesis. However, many studies suggest that the MM55 PON1 genotype is associated with a higher risk for Parkinson's disease in individuals exposed to organophosphates. In Alzheimer's disease most studies have failed to find any association between PON1 polymorphisms and the development of the disease. Some studies show that PON1 activity is decreased in patients with Alzheimer's disease or other dementias, suggesting a possible protective role of PON1. No links between PON1 polymorphisms or activity have been found in other neurodegenerative diseases such as multiple sclerosis and amyotrophic lateral sclerosis. PON1 is a potential player in the pathogenesis of several neurological disorders. More research is warranted to ascertain the precise pathogenic links and the prognostic value of its measurement in neurological patients.

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“…PON promoter and coding region polymorphisms were shown to be associated with increased stroke and coronary artery disease risk in several studies, 175,[182][183][184] but a recent study of the polymorphisms in PON I, PON II, and PON III in ischemic stroke patients showed no association with an increased risk of ischemic stroke. 185 …”

Section: Paraoxonase (Pon)mentioning

confidence: 99%

Redox Regulation in the Extracellular Environment

Ottaviano

Handy

Loscalzo

2008

Circ J

125

100

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Molecular oxygen is involved in the oxidation of substrates used to produce energy; however, normal metabolism can also generate harmful (bio)chemical byproducts. These deleterious products are partially reduced forms of oxygen, and include free radicals such as superoxide anion radical, hydroxyl radical, or highly oxidizing non-radical species such as hydrogen peroxide (H2O2) and lipid peroxides, which are collectively known as ROS. 1 ROS typically derive from normal metabolism, activated leukocytes, and ambient oxygen in the environment. The production and accumulation of ROS and their downstream effects can be controlled or attenuated by antioxidants. When the ability of antioxidants to eliminate harmful cellular and extracellular ROS is compromised, the balance between ROS generation and antioxidant function to eliminate ROS is shifted in favor of an accumulation of oxidants, which defines the state of oxidative stress in a cell or organism. Oxidative damage can affect DNA, lipids, and proteins, and eventually compromise cell integrity. Many studies have implicated ROS in the pathological processes leading to heart disease, cancer, aging, AIDS, and inflammatory and autoimmune diseases.Oxidants, especially free radicals, are highly reactive. Superoxide can react within milliseconds with nitric oxide (NO) to produce peroxynitrite (ONOO -), a reactive nitrogen species (RNS). The nitrosium cation and nitroxyl anion are other RNS derived from NO. 2 Peroxynitrite is a strong oxidant involved in the nitrosative modification of proteins and lipids. Owing to its rapid reaction with NO, superoxide may modulate NO bioavailability and, subsequently, regulate vascular function. 3 Circulation Journal Vol.72, January 2008The cytosol, mitochondria, peroxisomes, and plasma are all potential sites of ROS formation. 4 The major sources of ROS are enzymatic via nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (Nox), xanthine oxidase, myeloperoxidase, endothelial NO synthase (eNOS), or as a consequence of normal mitochondrial respiration. In vascular cells, other enzymatic sources of ROS include cytochrome P450 isoenzymes, lipoxygenase, cyclooxygenase, heme oxygenase, and glucose oxidase. 1,3,[5][6][7] Most reviews to date have focused on the role of intracellular antioxidants that eliminate ROS from the intracellular environment. There are, however, several extracellular antioxidants that also play an equally important role in limiting ROS accumulation in the extracellular environment. Along with limiting ROS accumulation, extracellular redox status is essential for maintaining protein stability and function.The major enzymes important for the elimination of extracellular H2O2 are glutathione peroxidase-3 (GPx-3) and peroxiredoxin IV (Prx IV). Other extracellular antioxidants involved in ROS elimination include paraoxonase (PON), thioredoxin (Trx), Trx reductase (TrxR), glutaredoxin (Grx), extracellular superoxide dismutase (EC-SOD), and extracellular glutathione (GSH).Some of these antioxidants, notably glutathione...

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Paraoxonase gene polymorphisms and haplotype analysis in a stroke population

Cited by 45 publications

References 42 publications

Genetic Polymorphism of Paraoxonase 3 Gene Ala99ala in Adjaandmahiethnic Groups in Benin.

Genetic Polymorphism of Paraoxonase 3 Gene Ala99ala in Adjaandmahiethnic Groups in Benin.

Paraoxonase 1 in neurological disorders

Redox Regulation in the Extracellular Environment

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