Table 1.
Demographic and clinical data of the healthy subjects and the ACS patients.
Table 2.
PON1 phenotypic distribution, activities, and oxidative stress markers in the healthy subjects and ACS patients.
Fig 1.
PON1 paraoxonase activities in the healthy subjects and the ACS patients based on their PON1 192 genotype.
The PON1 Q192R genotype was determined by RT-PCR. PON1 paraoxonase activity was determined by measuring paraoxon absorbance at 412 nm. Results are expressed as means ± SEM. *p<0.03 and ****p<0.0001 for comparison between ACS patients and healthy subjects with the same PON1 Q192R polymorphism or comparison between PON1 Q192R polymorphisms within the ACS group.
Fig 2.
PON1 paraoxonase activities in the healthy subjects and the ACS patients based on their PON1 55 genotype.
The PON1 L55M genotype was determined by RT-PCR. PON1 paraoxonase activity was determined by measuring paraoxon absorbance at 412 nm. Results are expressed as means ± SEM. ****p<0.0001 for comparison between ACS patients and healthy subjects with the same PON1 L55M polymorphism.
Fig 3.
Correlation between PON1 paraoxonase activity and the number of concomitant risk factors for CVD.
CVD risk factors: diabetes, obesity, high arterial blood pressure, alcohol, smoking, and family history. A Pearson correlation analysis was performed to assess the association between CVD risk factors and PON1 paraoxonase activity. H: Healthy, ACS: Acute Coronary Syndrome.
Table 3.
PON1 paraoxonase activity as a function of the health status of the participants.
Fig 4.
PON1 arylesterase activity in the healthy subjects and the ACS patients and based on their PON1 192 genotype.
The PON1 Q192R genotype was determined by RT-PCR. PON1 arylesterase activity was measured by the increase in absorbance at 270 using phenylacetate as a substrate. Results are expressed as means ± SEM. ** p<0.001 and ****p<0.0001 for the ACS patients compared to the healthy subjects with the same PON1 Q192R polymorphism.
Fig 5.
PON1 arylesterase activity in the healthy subjects and the ACS patients and based on their PON1 55 genotype.
The PON1 L55M genotype was determined by RT-PCR. PON1 arylesterase activity was measured by the increase in absorbance at 270 using phenylacetate as a substrate. Results are expressed as means ± SEM. *p<0.03, ** p<0.001 and ****p<0.0001 for the ACS patients compared to the healthy subjects with the same PON1 L55M polymorphism.
Table 4.
PON1 genotypic distribution and odds ratios of the genotype and alleles of the Q192R polymorphism in the healthy subjects and the ACS patients.
Table 5.
Genotype and allele frequencies of the L55M polymorphism.
Table 6.
PON1 55 and PON1 192 carrier frequencies of the 205 ACS patients.
Table 7.
Levels of biochemical parameters of PON1 55 and PON1 192 carriers in the ACS patient group.
Fig 6.
Comparison of the triglyceride levels of healthy subjects and ACS patients as a function of PON1 Q192R polymorphism.
***p<0.0001 and **** p<0.001 compared with the healthy subjects with the same PON1 Q192R polymorphism.
Fig 7.
Comparison of the triglyceride levels of healthy subjects and ACS patients as a function of PON1 L55M polymorphism.
**** p<0.001 compared with the healthy subjects with the same PON1 L55M polymorphism.