Reduced Postprandial Serum Paraoxonase Activity After a Meal Rich in Used Cooking Fat

Abstract

Abstract-Paraoxonase is an enzyme associated with HDL in human serum that hydrolyzes oxidized phospholipids and inhibits LDL oxidation, which is an important step in atherogenesis. In animals, addition of oxidized lipids to the circulation reduces paraoxonase activity, and diets rich in oxidized fat accelerate the development of atherosclerosis. The current randomized, crossover study was designed to compare the effect of a meal rich in oxidized lipids in the form of fat that had been used for deep-frying in a fast food restaurant and a control meal rich in the corresponding unused fat on postprandial serum paraoxonase (arylesterase) activity and peroxide content of LDL and its susceptibility to copper ion catalyzed oxidation in 12 healthy men. Four hours into the postprandial period, serum paraoxonase activity had decreased significantly after the used fat meal (Ϫ17%, Pϭ0.005) and had increased significantly after the meal rich in unused fat (14%, Pϭ0.005). These changes were significantly (Pϭ0.003) different. A time-course study indicated that serum paraoxonase activity remained lower than baseline for up to 8 hours after the used fat meal. Serum apoA1 concentration tended to decrease after the unused fat meal and tended to increase after the used fat meal. These changes were different at a marginal level of significance (Pϭ0.07). Also, a significantly (Pϭ0.03) greater decrease in apoA1 content of postprandial HDL was recorded after the unused fat meal. The peroxide content of LDL tended to decrease after the used fat meal and tended to increase after the control meal. These changes were significantly (Pϭ0.04) different. Susceptibility of isolated LDL to copper ion oxidation and plasma levels of malondialdehyde were unchanged during the study. These data suggest that in the postprandial period after a meal rich in used cooking fat, the enzymatic protection of LDL against accumulation of peroxides and atherogenic oxidative modification may be reduced, possibly due to factors associated with apoA1, without acutely affecting the intrinsic resistance of LDL to in vitro oxidation.

Paraoxonase 1 status in the Thai population

“…The results of stepwise multiple regression analysis confirmed that the HDL-C alone and apo AI together with the PON1 polymorphisms were significant contributors to the variation in serum PON1 activity towards phenylacetate and diazoxon, respectively. Additionally, the effects of environmental factors such as diet and exercise on serum PON1 activity have also been reported by several studies (Tomas et al 2001(Tomas et al , 2002Sutherland et al 1999;).…”

“…This variation is partly due to PON1 gene polymorphisms although nutritional, pharmacological and environmental factors also affect PON1 levels (Sutherland et al 1999;Paragh et al 2000;Balogh et al 2001). The PON1 gene has two major coding region polymorphisms due to amino acid substitutions at position 55 (leucine to methionine; L/M) and at position 192 (glutamine to arginine; Q/R) (Adkin et al 1993;Humbert et al 1993).…”

Oxidized Cholesterol in the Diet Accelerates the Development of Atherosclerosis in LDL Receptor– and Apolipoprotein E–Deficient Mice

“…Several mechanisms are possible, including the following: (1) oxidized cholesterol accelerates the use of antioxidants such as vitamin E, thereby increasing the ability of other pro-oxidants to oxidize fatty acids or lipoproteins; (2) oxidized cholesterol, when present in lipoproteins, may alter the lipoprotein structure, so that fatty acids are more exposed and therefore more prone to oxidation; (3) oxidized cholesterol may inhibit the action of enzymes such as paraoxonase that protect lipoproteins from being oxidized. 41,42 Most importantly, our results demonstrate that oxidized cholesterol in the diet increases fatty streak lesions in aortas of both LDLR-and apo E-deficient mice (Figure 4). In LDLR-deficient mice fed diets that contained oxidized cholesterol, fatty streak lesions increased from 15.93% to 21.00% (32% increase).…”

An antioxidant probiotic reduces postprandial lipemia and oxidative stress

“…PON is an antioxidant enzyme associated with HDL in human serum that hydrolyzes oxidized phospholipids and inhibits the LDL oxidation that is otherwise an important step in atherogenesis. In animals, the addition of oxidized lipids to the circulation reduces PON activity, and diets rich in oxidized fat accelerate the development of atherosclerosis [34]. Removal and inactivation of lipid peroxides which accumulate during LDL oxidation may be the central mechanism accounting for HDL antioxidative properties [35].…”