Table 1.
Tabulated representation of studies, worldwide, deciphering PON3 variants and investigating the role in coronary artery disease.
| Study | Subjects Enrolled | PON3 SNPs Studied | Outcome | Author, Year |
|---|---|---|---|---|
| Prospective Northwick Park Heart study II; to evaluate the effect of SNPs on CHD risk | 3052 healthy men | A99A (GCG to GCA) D107N (GAC) to (AAC) |
A99A SNP, did not revealed much information about its association with CAD but D107N was absent in the population. | Robertson et al. [50] (2003) |
| Polymorphisms screening of PON cluster in a Chinese Han population | 949 subjects in the 474 cases, 475 controls | −133 C>A | Not found significant effect on CHD risk but detected -133 C >A SNP in PON3 located at a potential binding site for transcription factor LFA-1(Integrin Lymphocyte Function-associated Antigen) | Wang et al. [53] (2003) |
| Identification of PON3 mutations in a population of Southern Italy | 1143 blood donors | G51G G73G A99A S311T G324D |
G51G, G73G, A99A were silent and S311T, G324D were missense mutations with no clarity on function in CAD development | Campo et al. [48] (2004) |
| PON gene cluster TagSNPs analysis—on illumina platform | 500 Caucasian males | PON1, PON2 and PON3 | No significant association with CAD disease | Carlson et al. [114] (2006) |
| Association study; PON3 with serum PON1 activity, risk of atherosclerosis in SLE cases | 377 cases and 482 controls (US whites and blacks) |
PON3 (A10340C, A2115T), PON1 (L55M, Q192R) |
All four SNPs explained 2%, 1%, 8%, and 19% of the variation in PON1 activity, respectively. PON3 SNPs described only 3% of variation in PON1 activity |
Sanghera et al. [51] (2008) |
| Influence of genetic polymorphisms of PON on lactonase activity | Healthy population |
PON3−567, PON3−665, PON3−746, PON3−4105, PON3−4970, PON3−4984 |
Lactonase activity was lower than Paraoxonase activity which indicated evaluation of liver function in clinics | Marsillach et al. [115] (2009) |
| PON3; concentration determination and its association analysis with promoter polymorphisms | n = 356; 156 women, 200 men; mean age: 47 years, of Caucasian from the Mediterranean region of Catalonia | (-567 C/T, -665 A/G, -746 C/T, -4105 G/A, -4970 T/G, -4984 A/G) | Promoter SNPs associated with PON3 serum concentration. TGTAGG, TGTGTA, CACGTA haplotypes were significantly associated with changes in serum PON3 concentration when adjusted for gender, age, BMI | Aragones et al. [52] (2011) |
| PON1 and PON3; atorvastatin hydrolysis | Blood and liver tissues of patients undergoing surgery(n = 150) | -4984A/G, -4105G/A, -1091A/G, -746C/T and F21F |
40 SNPs identified within the PON-locus associated with changes in atorvastatin δ-lactone hydrolysis and expression of PON1 but not PON3. Non genetic factors only were associated with PON3 expression | Riedmaier et al. [116] (2011) |
| Study of 51 common polymorphisms in the PON cluster | 1328 Caucasian males |
PON3 (rs17884000, rs9640632, rs468, rs11768074 rs10487132 rs740264) |
Predicted PON1 activity but not vascular disease | Daniel S. Kim et al. [117] (2012) |
| Case control study in North West Indian Punjabis | n = 300 cases, n = 300 proven CAD patients | C-133A, A99A, D107N, G324D | Low Paraoxonase 3 activity, circulatory concentration and A99A variants were predictive risks for angiographically proven CAD | K. Priyanka et al. [59] (2017) |