## 4 Discussion  
Several studies have documented the capacity of polyphenols to regulate PON1 transcription and its antioxidant effects. Polyphenolic compounds and flavonoids are found abundantly in some foods and in beverages such as red wine [13; 25; 29]. In the present study, the effect of dietary habits (macro- and micronutrients) and red wine on PON1 status in healthy population was evaluated. Our results showed that more than one half of the study participants were overweight or obese and that one-tenth of participants consumed tobacco or illicit drugs. Epidemiological studies have demonstrated that nutritional habits entertain a relationship with the onset of metabolic diseases [43]. A low intake of vegetables and fruits and a high intake of saturated fats predisposes to metabolic diseases. In this study, we requested that the participants did not change the normal diet that they had; however, we observed a significant decrease (8.7%; \(p<0.001\)) in caloric intake. Some studies have reported that alcohol consumption increases or decreases the blood levels of leptin, the hormone responsible for the sensation of satiety [44; 45; 46]. The effects of alcohol on leptin depend on the quantity, frequency of ingestion, and type of alcoholic beverage [47; 48; 49]. However, the effects of alcohol on the gastrointestinal signaling pathways have not been completely described given to that the mechanisms involved in satiety and food intake are complex [50; 51]. This also might explain the results observed in the intake of vitamins and minerals in our study population. The antioxidant compounds that are contained in some foods and red wine also regulate and protect PON1 from oxidation and could act synergistically or antagonistically with the enzyme [52]. Our data revealed a significant increase in the AREase specific activity by 18.97% (quotient of activity/PON1 protein concentration), after red wine consumption (\({}^{*}p<0.05\)). We observed differences in the activities of PON1 according to _Q192R_ genotype. The genotype distribution found in the current study was not different from that found in other Mexican populations [10; 53; 54; 55]. Few studies have reported PON1 specific activities. In this regard [PERSON] et al. [56] reported specific PON1 AREase (0.15 \(\pm\) 0.06 U/ng) and PONase (0.56 \(\pm\) 0.23 U/ug) activities in an Iranian population; and found a lower concentration of PON1, but higher AREase and PONase activities than the present study. [PERSON] et al. [55] reported that specific PON1 LACase activity is not influenced by PON1 polymorphism genetics. These results are in agreement with those found in this study, in which we did not observe in the LACase activity among the _Q192R_ genotypes either before or after red wine consumption. The relationship among the compounds contained in foods and the induction of PON1 is being thoroughly revised. Recent evidence deriving from in vitro, in vivo, and clinical observational studies suggests that PON1 activity is affected by the specific food profile intake [14; 57; 58]. Our results show that total fiber consumption increases PON1 specific AREase activity; contrariwise, [PERSON] et al. [59] reported decreases in PONase activity in healthy Finnish women with a high-fiber diet. Moreover, the beneficial antioxidant effects of vitamin E and its active compounds (primarily \(\alpha\)-, \(\beta\)-, \(\gamma\)- and \(\delta\)-tocopherols) in human health are well known [60]. However, our results have shown a negative association between specific AREase activity and the consumption of \(\beta\)-, \(\gamma\)- and \(\delta\)-tocopherols. [PERSON] et al. [61] reported failure in the antioxidant protection of tocopherols (\(\alpha\)- and \(\gamma\)-) on HDLs in vitro. As well, [PERSON] et al. [62] observed a decrease of 15.9 and 13.2% in PON1 AREase activity associated with HDL2 and HDL3, respectively, in healthy Irish volunteers whose uptake was of 400 IU of \(\alpha\)-tocopherol for 6 weeks.