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Addressing the link between paraoxonase-1 gene variants and the incidence of early onset myocardial infarction.

Rahman MF, Hashad IM, Abou-Aisha K, Abdel-Maksoud SM, Gad MZ - Arch Med Sci (2015)

Bottom Line: Allele frequencies were also significantly different between patients (Q = 62.75%, R = 37.25%) and controls (Q = 79.17%, R = 20.83%).The average PON/ARE ratio in MI patients (1.187 ±0.1) did not differ significantly from controls (1.118 ±0.26).PON1 192R allele represents an independent risk factor for early-onset AMI in Egyptians, and PON1 Q192R polymorphism modulates the paraoxonase phenotype.

View Article: PubMed Central - PubMed

Affiliation: Clinical Biochemistry Unit, Faculty of Pharmacy and Biotechnology, German University, Cairo, Egypt.

ABSTRACT

Introduction: The enzyme paraoxonase-1 (PON1) represents an endogenous defense mechanism against vascular oxidative stress, thereby contributing to the prevention of atherosclerosis. Several polymorphisms have been reported in the PON1 gene, including Q192R. PON1 phenotype is commonly expressed as the paraoxonase/arylesterase ratio (PON/ARE). The major aim of this study was to investigate the association between PON1 Q192R polymorphism, PON1 phenotypes and the incidence of early-onset acute myocardial infarction (AMI) in Egyptians.

Material and methods: The study subjects consisted of 102 AMI patients and 72 age-matched healthy controls. Genotyping and enzyme activities were determined using PCR-RFLP and kinetic spectrophotometric assays, respectively.

Results: The genotype distribution for the PON1 gene was significantly different between AMI patients (QQ = 38.24%, QR = 49.02%, RR = 12.75%) and controls (QQ = 66.67%, QR = 25%, RR = 8.33%). Allele frequencies were also significantly different between patients (Q = 62.75%, R = 37.25%) and controls (Q = 79.17%, R = 20.83%). The genotypes QR and RR showed higher risk for AMI compared to the homozygous QQ (odds ratio (OR) = 3.231, p < 0.001). The average PON/ARE ratio in MI patients (1.187 ±0.1) did not differ significantly from controls (1.118 ±0.26). However, it showed a significant difference among different genotypes in both AMI patients (QQ = 0.91 ±0.11, QR = 1.09 ±0.11 and RR = 2.65 ±0.4) (p = 0.0002) and controls (QQ = 0.68 ±0.1, QR = 1.07 ±0.11 and RR = 4.89 ±2.84) (p < 0.0001).

Conclusions: PON1 192R allele represents an independent risk factor for early-onset AMI in Egyptians, and PON1 Q192R polymorphism modulates the paraoxonase phenotype.

No MeSH data available.


Related in: MedlinePlus

The ARE activities among different genotypes in MI patients and controls. No significant difference was observed in the ARE activities among the different genotypes in both AMI patients (QQ = 79.56 ±6.62, QR = 69.08 ±4.73 and RR = 95.2 ±11.38 U/ml) (Kruskal-Wallis; p = 0.1170) and control subjects (QQ = 106.9 ±6.86, QR = 101.5 ±10.54 and RR = 86.28 ±31.62 U/ml) (Kruskal-Wallis; p = 0.8092)
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Figure 0005: The ARE activities among different genotypes in MI patients and controls. No significant difference was observed in the ARE activities among the different genotypes in both AMI patients (QQ = 79.56 ±6.62, QR = 69.08 ±4.73 and RR = 95.2 ±11.38 U/ml) (Kruskal-Wallis; p = 0.1170) and control subjects (QQ = 106.9 ±6.86, QR = 101.5 ±10.54 and RR = 86.28 ±31.62 U/ml) (Kruskal-Wallis; p = 0.8092)

Mentions: There was a significant difference in the PON activities among the different genotypes in both AMI patients (QQ = 60.88 ±6.36, QR = 69.66 ±6.56 and RR = 222.7 ±20.75 U/ml) (Kruskal-Wallis; p < 0.0001) and control subjects (QQ = 65.58 ±7.9, QR = 101.4 ±14.15 and RR = 206.6 ±53.65 U/ml) (Kruskal-Wallis; p = 0.0025) (Figure 4). No significant difference was observed in the ARE activities among the different genotypes in both AMI patients (QQ = 79.56 ±6.62, QR = 69.08 ±4.73 and RR = 95.2 ±11.38 U/ml) (Kruskal-Wallis; p = 0.1170) and control subjects (QQ = 106.9 ±6.86, QR = 101.5 ±10.54 and RR = 86.28 ±31.62 U/ml) (Kruskal-Wallis; p = 0.8092) (Figure 5). On the other hand, PON/ARE ratios showed a significant difference among different genotypes in both AMI patients (QQ = 0.91 ±0.11, QR = 1.09 ±0.11 and RR = 2.65 ±0.4) (Kruskal-Wallis; p = 0.0002) and control subjects (QQ = 0.68 ±0.1, QR = 1.07 ±0.11 and RR = 4.89 ±2.84) (Kruskal-Wallis; p < 0.0001) (Figure 6).


Addressing the link between paraoxonase-1 gene variants and the incidence of early onset myocardial infarction.

Rahman MF, Hashad IM, Abou-Aisha K, Abdel-Maksoud SM, Gad MZ - Arch Med Sci (2015)

The ARE activities among different genotypes in MI patients and controls. No significant difference was observed in the ARE activities among the different genotypes in both AMI patients (QQ = 79.56 ±6.62, QR = 69.08 ±4.73 and RR = 95.2 ±11.38 U/ml) (Kruskal-Wallis; p = 0.1170) and control subjects (QQ = 106.9 ±6.86, QR = 101.5 ±10.54 and RR = 86.28 ±31.62 U/ml) (Kruskal-Wallis; p = 0.8092)
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4495147&req=5

Figure 0005: The ARE activities among different genotypes in MI patients and controls. No significant difference was observed in the ARE activities among the different genotypes in both AMI patients (QQ = 79.56 ±6.62, QR = 69.08 ±4.73 and RR = 95.2 ±11.38 U/ml) (Kruskal-Wallis; p = 0.1170) and control subjects (QQ = 106.9 ±6.86, QR = 101.5 ±10.54 and RR = 86.28 ±31.62 U/ml) (Kruskal-Wallis; p = 0.8092)
Mentions: There was a significant difference in the PON activities among the different genotypes in both AMI patients (QQ = 60.88 ±6.36, QR = 69.66 ±6.56 and RR = 222.7 ±20.75 U/ml) (Kruskal-Wallis; p < 0.0001) and control subjects (QQ = 65.58 ±7.9, QR = 101.4 ±14.15 and RR = 206.6 ±53.65 U/ml) (Kruskal-Wallis; p = 0.0025) (Figure 4). No significant difference was observed in the ARE activities among the different genotypes in both AMI patients (QQ = 79.56 ±6.62, QR = 69.08 ±4.73 and RR = 95.2 ±11.38 U/ml) (Kruskal-Wallis; p = 0.1170) and control subjects (QQ = 106.9 ±6.86, QR = 101.5 ±10.54 and RR = 86.28 ±31.62 U/ml) (Kruskal-Wallis; p = 0.8092) (Figure 5). On the other hand, PON/ARE ratios showed a significant difference among different genotypes in both AMI patients (QQ = 0.91 ±0.11, QR = 1.09 ±0.11 and RR = 2.65 ±0.4) (Kruskal-Wallis; p = 0.0002) and control subjects (QQ = 0.68 ±0.1, QR = 1.07 ±0.11 and RR = 4.89 ±2.84) (Kruskal-Wallis; p < 0.0001) (Figure 6).

Bottom Line: Allele frequencies were also significantly different between patients (Q = 62.75%, R = 37.25%) and controls (Q = 79.17%, R = 20.83%).The average PON/ARE ratio in MI patients (1.187 ±0.1) did not differ significantly from controls (1.118 ±0.26).PON1 192R allele represents an independent risk factor for early-onset AMI in Egyptians, and PON1 Q192R polymorphism modulates the paraoxonase phenotype.

View Article: PubMed Central - PubMed

Affiliation: Clinical Biochemistry Unit, Faculty of Pharmacy and Biotechnology, German University, Cairo, Egypt.

ABSTRACT

Introduction: The enzyme paraoxonase-1 (PON1) represents an endogenous defense mechanism against vascular oxidative stress, thereby contributing to the prevention of atherosclerosis. Several polymorphisms have been reported in the PON1 gene, including Q192R. PON1 phenotype is commonly expressed as the paraoxonase/arylesterase ratio (PON/ARE). The major aim of this study was to investigate the association between PON1 Q192R polymorphism, PON1 phenotypes and the incidence of early-onset acute myocardial infarction (AMI) in Egyptians.

Material and methods: The study subjects consisted of 102 AMI patients and 72 age-matched healthy controls. Genotyping and enzyme activities were determined using PCR-RFLP and kinetic spectrophotometric assays, respectively.

Results: The genotype distribution for the PON1 gene was significantly different between AMI patients (QQ = 38.24%, QR = 49.02%, RR = 12.75%) and controls (QQ = 66.67%, QR = 25%, RR = 8.33%). Allele frequencies were also significantly different between patients (Q = 62.75%, R = 37.25%) and controls (Q = 79.17%, R = 20.83%). The genotypes QR and RR showed higher risk for AMI compared to the homozygous QQ (odds ratio (OR) = 3.231, p < 0.001). The average PON/ARE ratio in MI patients (1.187 ±0.1) did not differ significantly from controls (1.118 ±0.26). However, it showed a significant difference among different genotypes in both AMI patients (QQ = 0.91 ±0.11, QR = 1.09 ±0.11 and RR = 2.65 ±0.4) (p = 0.0002) and controls (QQ = 0.68 ±0.1, QR = 1.07 ±0.11 and RR = 4.89 ±2.84) (p < 0.0001).

Conclusions: PON1 192R allele represents an independent risk factor for early-onset AMI in Egyptians, and PON1 Q192R polymorphism modulates the paraoxonase phenotype.

No MeSH data available.


Related in: MedlinePlus