The analysis of PON1 promoter T(-107)C genotype frequencies showed a greater percentage of subjects with the (-107)CC genotype (27%) among octogenarians compared with the (-107)CC genotype found in the controls (14%). PCR amplification of the PON1 T(-107)C polymorphism was performed with the following primers: sense 5' AGCTAGCTGCGGACCCGGCGGGGAGGaG3' and reverse 5' GGC TGCAGCCCTCACCACAACCC30', (annealing temperature: 67°C). The lowercase base in PON1 (-107) upstream primer indicates a mismatch, introducing a restriction site for BseBI enzyme (New England Bio Labs, Cambridge, UK), because there is no specific restriction site cutting the DNA original sequence. After digestion, the (-107)C allele was identified by 28- and 212-bp fragments, whereas the (-107)T allele resulted in a non-digested 240-bp fragment.

Categorical variables among paraoxonase genotypes were compared by x^2 test. Allele frequencies were...

Table 3 shows serum PON1 activity and PON1 promoter T(-107)C and coding region Leu55Met and Gln192Arg polymorphisms. Multiple regression analysis of age demonstrated that besides the T(-107)C promoter polymorphism, HDL-C and PON1 activity entered in the model, thus indicating an association between the PON1 promoter T(-107)C polymorphisms, HDL-C levels, PON1 activity and longevity. 

No difference in the L55M and Q192R genotypes distribution was found in both groups. For the first time, our results show that the PON1 gene promoter T(-107)C polymorphism could significantly affect the resistance to develop cardiovascular disorders in old subjects. A significantly higher percentage of subjects with the (-107)CC genotype was found among the octogenarians compared with controls; the (-107)CC genotype was associated with higher PON1 activity and plasma HDL levels than (-107)TT genotype. Linkage disequilibrium was observed between the PON1 promoter T(-107)C and L55M coding region (χ^2=33.34; P<0.001) polymorphisms and between L55M and QStudies have failed to find an association between PON1 genotype and lipid profile (Nevin et al., 1996; Xia et al., 2003). However, genetic variations in PON1 have been found to be associated with variation in plasma lipoprotein traits (Saha et al., 1991; Hegele et al., 1995). Although the function of paraoxonase in lipoprotein metabolism remains an unanswered question, our data could support the suggestion that the PON1 gene may be a determinant of plasma lipoproteins. Further investigations are needed to clarify this assumption. Conversely, beneficial factors affecting HDL, such as diet, gender, and lifestyle, would be expected to influence HDL composition. 

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